bdnf prodomain  (Alomone Labs)


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    Structured Review

    Alomone Labs bdnf prodomain
    <t>BDNF</t> <t>prodomain</t> in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.
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    Images

    1) Product Images from "ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses"

    Article Title: ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2022.866802

    BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.

    Techniques Used: Concentration Assay, Inhibition

    BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.
    Figure Legend Snippet: BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.

    Techniques Used: Inhibition

    BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.

    Techniques Used: Inhibition

    p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.
    Figure Legend Snippet: p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.

    Techniques Used: Inhibition, Transmission Assay, Activity Assay, Mouse Assay

    2) Product Images from "ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses"

    Article Title: ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2022.866802

    BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.

    Techniques Used: Concentration Assay, Inhibition

    BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.
    Figure Legend Snippet: BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.

    Techniques Used: Inhibition

    BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.

    Techniques Used: Inhibition

    p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.
    Figure Legend Snippet: p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.

    Techniques Used: Inhibition, Transmission Assay, Activity Assay, Mouse Assay

    3) Product Images from "ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses"

    Article Title: ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2022.866802

    BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.

    Techniques Used: Concentration Assay, Inhibition

    BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.
    Figure Legend Snippet: BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.

    Techniques Used: Inhibition

    BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.

    Techniques Used: Inhibition

    p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.
    Figure Legend Snippet: p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.

    Techniques Used: Inhibition, Transmission Assay, Activity Assay, Mouse Assay

    4) Product Images from "ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses"

    Article Title: ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2022.866802

    BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.

    Techniques Used: Concentration Assay, Inhibition

    BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.
    Figure Legend Snippet: BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.

    Techniques Used: Inhibition

    BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.

    Techniques Used: Inhibition

    p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.
    Figure Legend Snippet: p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.

    Techniques Used: Inhibition, Transmission Assay, Activity Assay, Mouse Assay

    5) Product Images from "ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses"

    Article Title: ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2022.866802

    BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.

    Techniques Used: Concentration Assay, Inhibition

    BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.
    Figure Legend Snippet: BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.

    Techniques Used: Inhibition

    BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.

    Techniques Used: Inhibition

    p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.
    Figure Legend Snippet: p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.

    Techniques Used: Inhibition, Transmission Assay, Activity Assay, Mouse Assay

    6) Product Images from "ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses"

    Article Title: ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2022.866802

    BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.

    Techniques Used: Concentration Assay, Inhibition

    BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.
    Figure Legend Snippet: BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.

    Techniques Used: Inhibition

    BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.

    Techniques Used: Inhibition

    p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.
    Figure Legend Snippet: p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.

    Techniques Used: Inhibition, Transmission Assay, Activity Assay, Mouse Assay

    7) Product Images from "ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses"

    Article Title: ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2022.866802

    BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.

    Techniques Used: Concentration Assay, Inhibition

    BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.
    Figure Legend Snippet: BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.

    Techniques Used: Inhibition

    BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.

    Techniques Used: Inhibition

    p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.
    Figure Legend Snippet: p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.

    Techniques Used: Inhibition, Transmission Assay, Activity Assay, Mouse Assay

    8) Product Images from "ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses"

    Article Title: ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2022.866802

    BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.

    Techniques Used: Concentration Assay, Inhibition

    BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.
    Figure Legend Snippet: BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.

    Techniques Used: Inhibition

    BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.

    Techniques Used: Inhibition

    p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.
    Figure Legend Snippet: p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.

    Techniques Used: Inhibition, Transmission Assay, Activity Assay, Mouse Assay

    9) Product Images from "ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses"

    Article Title: ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2022.866802

    BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.

    Techniques Used: Concentration Assay, Inhibition

    BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.
    Figure Legend Snippet: BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.

    Techniques Used: Inhibition

    BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.

    Techniques Used: Inhibition

    p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.
    Figure Legend Snippet: p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.

    Techniques Used: Inhibition, Transmission Assay, Activity Assay, Mouse Assay

    10) Product Images from "Astrocytic microdomains from mouse cortex gain molecular control over long-term information storage and memory retention"

    Article Title: Astrocytic microdomains from mouse cortex gain molecular control over long-term information storage and memory retention

    Journal: Communications Biology

    doi: 10.1038/s42003-021-02678-x

    astrocytic BDNFpro secretion rescues LTP deficit in p75-flox mice. a Schematic representation of the experimental design. Step I, deletion of p75 NTR in astrocytes from tamoxifen-treated p75-flox mice precludes proBDNF transfer from neurons to astrocyte following TBS. Step II, LV-BDNFpro stop transduction replaces BDNFpro in astrocytes. Schematic representation of the experimental paradigms (right); mice were treated with tamoxifen (−5 to 0), injected with lentiviruses the last day of tamoxifen treatment (0 dptm) and finally recorded (14 dptm). LTP evoked in slices from p75-flox mice and control littermates injected with LV-GFP stop or LV-BDNFpro stop is shown. *** p
    Figure Legend Snippet: astrocytic BDNFpro secretion rescues LTP deficit in p75-flox mice. a Schematic representation of the experimental design. Step I, deletion of p75 NTR in astrocytes from tamoxifen-treated p75-flox mice precludes proBDNF transfer from neurons to astrocyte following TBS. Step II, LV-BDNFpro stop transduction replaces BDNFpro in astrocytes. Schematic representation of the experimental paradigms (right); mice were treated with tamoxifen (−5 to 0), injected with lentiviruses the last day of tamoxifen treatment (0 dptm) and finally recorded (14 dptm). LTP evoked in slices from p75-flox mice and control littermates injected with LV-GFP stop or LV-BDNFpro stop is shown. *** p

    Techniques Used: Mouse Assay, Transduction, Injection

    BDNFpro restores memory retention in p75-flox mice. a Schematic diagram depicting the behavioral paradigm used for ORT. Mice were subjected to familiarization (sample phase) with two identical objects (circles). A test phase in which one familiar object (circle) is substituted with a novel one was performed after 10 min (square) and 24 h (triangle). b Schematic diagram depicting the experimental paradigm. p75-flox mice and control littermates treated with tamoxifen (−5 to 0) and injected with LV-GFP stop or LV-BDNFpro stop the last day of tamoxifen treatment (0 dptm) were subjected to ORT (14 dptm). Discrimination index is plotted against time interval between sample phase and test phases. ** p
    Figure Legend Snippet: BDNFpro restores memory retention in p75-flox mice. a Schematic diagram depicting the behavioral paradigm used for ORT. Mice were subjected to familiarization (sample phase) with two identical objects (circles). A test phase in which one familiar object (circle) is substituted with a novel one was performed after 10 min (square) and 24 h (triangle). b Schematic diagram depicting the experimental paradigm. p75-flox mice and control littermates treated with tamoxifen (−5 to 0) and injected with LV-GFP stop or LV-BDNFpro stop the last day of tamoxifen treatment (0 dptm) were subjected to ORT (14 dptm). Discrimination index is plotted against time interval between sample phase and test phases. ** p

    Techniques Used: Mouse Assay, Injection

    post-synaptic targeting of TrkB/SorCS2 complex. a Schematic representation of the experimental design. Circular DNA probes (−) and (+) are coupled to II° antibody targeting αSorCS2 and αTrkB I° antibody. BDNFpro induces TrkB/SorCS2 complex formation (PLA TrkB/SorCS2 ) that is prevented in the presence of αSorCS2 (blocking) antibody. b Panels show PLA TrkB/SorCS2 signals in primary culture of cortical neurons treated with vehicle or BDNFpro. The insets show reference GFP-neurons. Scale bars: 5 μm. c Panels show a GFP-neuron treated with BDNFpro. Scale bar: 5 μm. Magnification of regions of interest 1 and 2 shows dendritic PLA TrkB/SorCS2 localization (red arrowheads). Scale bar: 1 μm. d Quantification of PLA TrkB/SorCS2 signal in cultured neurons treated with vehicle, BDNFpro (in presence or absence of αSorCS2), mBDNF or proBDNF CR . Data are presented as mean ± SEM; ** p
    Figure Legend Snippet: post-synaptic targeting of TrkB/SorCS2 complex. a Schematic representation of the experimental design. Circular DNA probes (−) and (+) are coupled to II° antibody targeting αSorCS2 and αTrkB I° antibody. BDNFpro induces TrkB/SorCS2 complex formation (PLA TrkB/SorCS2 ) that is prevented in the presence of αSorCS2 (blocking) antibody. b Panels show PLA TrkB/SorCS2 signals in primary culture of cortical neurons treated with vehicle or BDNFpro. The insets show reference GFP-neurons. Scale bars: 5 μm. c Panels show a GFP-neuron treated with BDNFpro. Scale bar: 5 μm. Magnification of regions of interest 1 and 2 shows dendritic PLA TrkB/SorCS2 localization (red arrowheads). Scale bar: 1 μm. d Quantification of PLA TrkB/SorCS2 signal in cultured neurons treated with vehicle, BDNFpro (in presence or absence of αSorCS2), mBDNF or proBDNF CR . Data are presented as mean ± SEM; ** p

    Techniques Used: Proximity Ligation Assay, Blocking Assay, Cell Culture

    BDNFpro-induced TrkB/SorCS2 targeting. a Schematic representation of the experimental design. Step I, deletion of p75 NTR in astrocytes from tamoxifen-treated p75-flox mice precludes proBDNF transfer from neurons to astrocyte following TBS. Step II, LV-BDNFpro stop transduction replaces BDNFpro in astrocytes. Step III, astrocytic BDNFpro provides final increase of TrkB/SorCS2 complexes in dendritic spines and LTP maintenance. b z-stack reconstruction showing NeuN/PLA TrkB/SorCS2 colocalization signal in TBS-slices from p75-flox mice transduced with LV-GFP stop or LV-BDNFpro stop . Scale bars: 40 μm. The insets show the field of analysis. Scale bars: 15 μm. NeuN/PLA TrkB/SorCS2 colocalization was quantified using Mander’s overlap. ** p
    Figure Legend Snippet: BDNFpro-induced TrkB/SorCS2 targeting. a Schematic representation of the experimental design. Step I, deletion of p75 NTR in astrocytes from tamoxifen-treated p75-flox mice precludes proBDNF transfer from neurons to astrocyte following TBS. Step II, LV-BDNFpro stop transduction replaces BDNFpro in astrocytes. Step III, astrocytic BDNFpro provides final increase of TrkB/SorCS2 complexes in dendritic spines and LTP maintenance. b z-stack reconstruction showing NeuN/PLA TrkB/SorCS2 colocalization signal in TBS-slices from p75-flox mice transduced with LV-GFP stop or LV-BDNFpro stop . Scale bars: 40 μm. The insets show the field of analysis. Scale bars: 15 μm. NeuN/PLA TrkB/SorCS2 colocalization was quantified using Mander’s overlap. ** p

    Techniques Used: Mouse Assay, Transduction, Proximity Ligation Assay

    BDNFpro expression in cortical astrocytes. a Schematic representation of proBDNF precursor and cleaved BDNFpro domain. αBDNFpro antibody recognizes the furin cleavage site of the prodomain. Western blotting probing recombinant mBDNF, BDNFpro, and proBDNF CR with αBDNFpro and αmBDNF antibodies. b Cortical slices from control mice injected with AAV-GFAP-GFP virus were recorded and fixed 10 min after TBS for immunostaining. z-stack reconstruction shows astrocytes labeled by GFP. Magnification of a single stack from a region of interest (ROI) shows BDNFpro immunoreactivity and BDNFpro/GFP colocalization signal of one GFP-astrocyte delimited by an approximate territory (white dashed). Scale bars: 10 µm. c z-stack reconstruction of BDNFpro/GFP colocalization signals in astrocytes from baseline- and TBS-slices from control mice. The insets show GFP signal. BDNFpro/GFP colocalization was quantified in the whole cell and branches using Mander’s overlap. *** p
    Figure Legend Snippet: BDNFpro expression in cortical astrocytes. a Schematic representation of proBDNF precursor and cleaved BDNFpro domain. αBDNFpro antibody recognizes the furin cleavage site of the prodomain. Western blotting probing recombinant mBDNF, BDNFpro, and proBDNF CR with αBDNFpro and αmBDNF antibodies. b Cortical slices from control mice injected with AAV-GFAP-GFP virus were recorded and fixed 10 min after TBS for immunostaining. z-stack reconstruction shows astrocytes labeled by GFP. Magnification of a single stack from a region of interest (ROI) shows BDNFpro immunoreactivity and BDNFpro/GFP colocalization signal of one GFP-astrocyte delimited by an approximate territory (white dashed). Scale bars: 10 µm. c z-stack reconstruction of BDNFpro/GFP colocalization signals in astrocytes from baseline- and TBS-slices from control mice. The insets show GFP signal. BDNFpro/GFP colocalization was quantified in the whole cell and branches using Mander’s overlap. *** p

    Techniques Used: Expressing, Western Blot, Recombinant, Mouse Assay, Injection, Immunostaining, Labeling

    subcellular localization of BDNFpro. a Graphical representation of the SIM super-resolution microscope. 3D-SIM image of a GFP-labeled astrocyte in a TBS-slice from control mice. Scale bar: 10 µm. Magnification of a ROI shows BDNFpro/GFP colocalization signal localized in fine membrane extensions of the cell periphery. Scale bar: 200 nm. b 3D-SIM image of the ROI in ( a ); z-axe is visualized in pseudocolor to facilitate microdomains identification. Scale bar: 200 nm. Magnification of microdomains characterized by the typical fingerlike extension (dashed squares 1 and 2) and flat lamellar sheath (dashed squares 3 and 4) are shown. BDNFpro/GFP colocalization is indicated (red arrowheads). Scale bars: 40 nm.
    Figure Legend Snippet: subcellular localization of BDNFpro. a Graphical representation of the SIM super-resolution microscope. 3D-SIM image of a GFP-labeled astrocyte in a TBS-slice from control mice. Scale bar: 10 µm. Magnification of a ROI shows BDNFpro/GFP colocalization signal localized in fine membrane extensions of the cell periphery. Scale bar: 200 nm. b 3D-SIM image of the ROI in ( a ); z-axe is visualized in pseudocolor to facilitate microdomains identification. Scale bar: 200 nm. Magnification of microdomains characterized by the typical fingerlike extension (dashed squares 1 and 2) and flat lamellar sheath (dashed squares 3 and 4) are shown. BDNFpro/GFP colocalization is indicated (red arrowheads). Scale bars: 40 nm.

    Techniques Used: Microscopy, Labeling, Mouse Assay

    vesicular localization of BDNFpro. a z-stack reconstruction shows astrocytes labeled by GFP. Cortical slices from control mice injected with AAV-GFAP-GFP virus were fixed 10 min after TBS and processed for immunostaining and confocal analysis. Scale bar: 10 µm. Magnification of a ROI shows one GFP-astrocyte delimited by an approximate territory (white dashed). Scale bar: 10 µm. BDNFpro/GFP and Vamp2/GFP co-localizations signals are shown. Magnification shows representative areas (dashed squares 1 to 4) in which BDNFpro/GFP and Vamp2/GFP signals overlap. Scale bars: 1 µm. b 3D-SIM image of a GFP-labeled astrocyte in a TBS-slice from control mice. Scale bar: 10 µm. Magnification of a ROI shows BDNFpro/Vamp2 colocalization signal. Scale bar: 500 nm. Magnification shows BDNFpro/Vamp2 colocalization signal in fine membrane extensions of the cell periphery (dashed squares 1 to 4). Scale bars: 50 nm. c EM image depicts BDNFpro-gold at astrocytic microdomains (light blue) surrounding an axon bouton. Scale bar: 100 nm. Magnification of the ROI shows gold particles (red arrowheads) in vesicular-like structures. Scale bar: 20 nm. d Digital reconstruction of the image in ( c ). Astrocytic vesicles (black boundary) are shown.
    Figure Legend Snippet: vesicular localization of BDNFpro. a z-stack reconstruction shows astrocytes labeled by GFP. Cortical slices from control mice injected with AAV-GFAP-GFP virus were fixed 10 min after TBS and processed for immunostaining and confocal analysis. Scale bar: 10 µm. Magnification of a ROI shows one GFP-astrocyte delimited by an approximate territory (white dashed). Scale bar: 10 µm. BDNFpro/GFP and Vamp2/GFP co-localizations signals are shown. Magnification shows representative areas (dashed squares 1 to 4) in which BDNFpro/GFP and Vamp2/GFP signals overlap. Scale bars: 1 µm. b 3D-SIM image of a GFP-labeled astrocyte in a TBS-slice from control mice. Scale bar: 10 µm. Magnification of a ROI shows BDNFpro/Vamp2 colocalization signal. Scale bar: 500 nm. Magnification shows BDNFpro/Vamp2 colocalization signal in fine membrane extensions of the cell periphery (dashed squares 1 to 4). Scale bars: 50 nm. c EM image depicts BDNFpro-gold at astrocytic microdomains (light blue) surrounding an axon bouton. Scale bar: 100 nm. Magnification of the ROI shows gold particles (red arrowheads) in vesicular-like structures. Scale bar: 20 nm. d Digital reconstruction of the image in ( c ). Astrocytic vesicles (black boundary) are shown.

    Techniques Used: Labeling, Mouse Assay, Injection, Immunostaining

    localization of BDNFpro in astrocytic microdomains. a Experimental design linking field-potential with electron microscopy (EM) in layer II/III perirhinal cortex. TBS (10 min)-slices were dissected for EM processing. b Representative EM-image depicts BDNFpro-gold particles at axon bouton (dashed squares 1 to 4) and dendritic spine (dashed squares 5 and 6). Scale bar: 100 nm. Magnification indicates representative areas (dashed squares 1 to 6) in which gold particles (red arrowheads) localization is shown. Scale bars: 10 nm. c Representative EM-image depicts BDNFpro-gold particles (dashed squares 1 to 6) at astrocytic microdomains (light blue) Scale bar: 250 nm. Magnification indicates representative areas (dashed squares 1 to 6) in which gold particles (red arrowheads) localization is shown. Scale bars: 20 nm. d Dot plot depicts the number of BDNFpro-gold particles in whole astrocytes and peri-synaptic astrocytes counted per section ( n = 41 sections, 5 slices, 3 mice). e Dot plot depicts the percentage of BDNFpro-gold particles at peri-synaptic astrocytes ( n = 41 sections, 5 slices, 3 mice). Data are mean ± SEM.
    Figure Legend Snippet: localization of BDNFpro in astrocytic microdomains. a Experimental design linking field-potential with electron microscopy (EM) in layer II/III perirhinal cortex. TBS (10 min)-slices were dissected for EM processing. b Representative EM-image depicts BDNFpro-gold particles at axon bouton (dashed squares 1 to 4) and dendritic spine (dashed squares 5 and 6). Scale bar: 100 nm. Magnification indicates representative areas (dashed squares 1 to 6) in which gold particles (red arrowheads) localization is shown. Scale bars: 10 nm. c Representative EM-image depicts BDNFpro-gold particles (dashed squares 1 to 6) at astrocytic microdomains (light blue) Scale bar: 250 nm. Magnification indicates representative areas (dashed squares 1 to 6) in which gold particles (red arrowheads) localization is shown. Scale bars: 20 nm. d Dot plot depicts the number of BDNFpro-gold particles in whole astrocytes and peri-synaptic astrocytes counted per section ( n = 41 sections, 5 slices, 3 mice). e Dot plot depicts the percentage of BDNFpro-gold particles at peri-synaptic astrocytes ( n = 41 sections, 5 slices, 3 mice). Data are mean ± SEM.

    Techniques Used: Electron Microscopy, Mouse Assay

    11) Product Images from "ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses"

    Article Title: ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2022.866802

    BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.

    Techniques Used: Concentration Assay, Inhibition

    BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.
    Figure Legend Snippet: BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.

    Techniques Used: Inhibition

    BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.

    Techniques Used: Inhibition

    p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.
    Figure Legend Snippet: p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.

    Techniques Used: Inhibition, Transmission Assay, Activity Assay, Mouse Assay

    12) Product Images from "ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses"

    Article Title: ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2022.866802

    BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.

    Techniques Used: Concentration Assay, Inhibition

    BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.
    Figure Legend Snippet: BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.

    Techniques Used: Inhibition

    BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.

    Techniques Used: Inhibition

    p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.
    Figure Legend Snippet: p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.

    Techniques Used: Inhibition, Transmission Assay, Activity Assay, Mouse Assay

    13) Product Images from "ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses"

    Article Title: ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2022.866802

    BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.

    Techniques Used: Concentration Assay, Inhibition

    BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.
    Figure Legend Snippet: BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.

    Techniques Used: Inhibition

    BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.

    Techniques Used: Inhibition

    p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.
    Figure Legend Snippet: p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.

    Techniques Used: Inhibition, Transmission Assay, Activity Assay, Mouse Assay

    14) Product Images from "ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses"

    Article Title: ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2022.866802

    BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.

    Techniques Used: Concentration Assay, Inhibition

    BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.
    Figure Legend Snippet: BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.

    Techniques Used: Inhibition

    BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.

    Techniques Used: Inhibition

    p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.
    Figure Legend Snippet: p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.

    Techniques Used: Inhibition, Transmission Assay, Activity Assay, Mouse Assay

    15) Product Images from "ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses"

    Article Title: ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2022.866802

    BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.

    Techniques Used: Concentration Assay, Inhibition

    BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.
    Figure Legend Snippet: BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.

    Techniques Used: Inhibition

    BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.

    Techniques Used: Inhibition

    p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.
    Figure Legend Snippet: p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.

    Techniques Used: Inhibition, Transmission Assay, Activity Assay, Mouse Assay

    16) Product Images from "ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses"

    Article Title: ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2022.866802

    BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.

    Techniques Used: Concentration Assay, Inhibition

    BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.
    Figure Legend Snippet: BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.

    Techniques Used: Inhibition

    BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.

    Techniques Used: Inhibition

    p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.
    Figure Legend Snippet: p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.

    Techniques Used: Inhibition, Transmission Assay, Activity Assay, Mouse Assay

    17) Product Images from "ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses"

    Article Title: ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2022.866802

    BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.

    Techniques Used: Concentration Assay, Inhibition

    BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.
    Figure Legend Snippet: BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.

    Techniques Used: Inhibition

    BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.

    Techniques Used: Inhibition

    p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.
    Figure Legend Snippet: p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.

    Techniques Used: Inhibition, Transmission Assay, Activity Assay, Mouse Assay

    18) Product Images from "ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses"

    Article Title: ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2022.866802

    BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.

    Techniques Used: Concentration Assay, Inhibition

    BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.
    Figure Legend Snippet: BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.

    Techniques Used: Inhibition

    BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.

    Techniques Used: Inhibition

    p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.
    Figure Legend Snippet: p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.

    Techniques Used: Inhibition, Transmission Assay, Activity Assay, Mouse Assay

    19) Product Images from "ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses"

    Article Title: ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2022.866802

    BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.

    Techniques Used: Concentration Assay, Inhibition

    BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.
    Figure Legend Snippet: BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.

    Techniques Used: Inhibition

    BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.

    Techniques Used: Inhibition

    p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.
    Figure Legend Snippet: p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.

    Techniques Used: Inhibition, Transmission Assay, Activity Assay, Mouse Assay

    20) Product Images from "Identification of a Linear Epitope in Sortilin That Partakes in Pro-neurotrophin Binding *"

    Article Title: Identification of a Linear Epitope in Sortilin That Partakes in Pro-neurotrophin Binding *

    Journal: The Journal of Biological Chemistry

    doi: 10.1074/jbc.M109.062364

    Differential binding of pro-BDNF and neurotension to sortilin and pro-sortilin. A , SPR analysis showing that unprocessed pro-BDNF (50 n m ) binds nearly as efficiently to the receptor in the presence (pro-sortilin) as in the absence (sortilin) of the receptor
    Figure Legend Snippet: Differential binding of pro-BDNF and neurotension to sortilin and pro-sortilin. A , SPR analysis showing that unprocessed pro-BDNF (50 n m ) binds nearly as efficiently to the receptor in the presence (pro-sortilin) as in the absence (sortilin) of the receptor

    Techniques Used: Binding Assay, SPR Assay

    Selective competition of ligands by sortilin-derived peptide antagonist. SPR binding analysis of 50 n m unprocessed pro-BDNF ( A ), 50 n m unprocessed pro-NGF ( B ), and 90 n m RAP ( C ) to immobilized sortilin in the absence and presence of the sort166–181
    Figure Legend Snippet: Selective competition of ligands by sortilin-derived peptide antagonist. SPR binding analysis of 50 n m unprocessed pro-BDNF ( A ), 50 n m unprocessed pro-NGF ( B ), and 90 n m RAP ( C ) to immobilized sortilin in the absence and presence of the sort166–181

    Techniques Used: Derivative Assay, SPR Assay, Binding Assay

    Mutation of the linear binding site specifically impairs binding of both the NGF and the BDNF pro-domains. SPR analysis showing reduced binding of equal amounts (analyte concentration: 200 n m ) of the soluble extracellular domains of sortilin-4A compared
    Figure Legend Snippet: Mutation of the linear binding site specifically impairs binding of both the NGF and the BDNF pro-domains. SPR analysis showing reduced binding of equal amounts (analyte concentration: 200 n m ) of the soluble extracellular domains of sortilin-4A compared

    Techniques Used: Mutagenesis, Binding Assay, SPR Assay, Concentration Assay

    21) Product Images from "ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses"

    Article Title: ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2022.866802

    BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.

    Techniques Used: Concentration Assay, Inhibition

    BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.
    Figure Legend Snippet: BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.

    Techniques Used: Inhibition

    BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.

    Techniques Used: Inhibition

    p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.
    Figure Legend Snippet: p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.

    Techniques Used: Inhibition, Transmission Assay, Activity Assay, Mouse Assay

    22) Product Images from "ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses"

    Article Title: ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2022.866802

    BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.

    Techniques Used: Concentration Assay, Inhibition

    BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.
    Figure Legend Snippet: BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.

    Techniques Used: Inhibition

    BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.

    Techniques Used: Inhibition

    p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.
    Figure Legend Snippet: p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.

    Techniques Used: Inhibition, Transmission Assay, Activity Assay, Mouse Assay

    23) Product Images from "ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses"

    Article Title: ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2022.866802

    BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.

    Techniques Used: Concentration Assay, Inhibition

    BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.
    Figure Legend Snippet: BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.

    Techniques Used: Inhibition

    BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.

    Techniques Used: Inhibition

    p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.
    Figure Legend Snippet: p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.

    Techniques Used: Inhibition, Transmission Assay, Activity Assay, Mouse Assay

    24) Product Images from "ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses"

    Article Title: ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2022.866802

    BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.

    Techniques Used: Concentration Assay, Inhibition

    BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.
    Figure Legend Snippet: BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.

    Techniques Used: Inhibition

    BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.

    Techniques Used: Inhibition

    p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.
    Figure Legend Snippet: p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.

    Techniques Used: Inhibition, Transmission Assay, Activity Assay, Mouse Assay

    25) Product Images from "ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses"

    Article Title: ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2022.866802

    BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.

    Techniques Used: Concentration Assay, Inhibition

    BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.
    Figure Legend Snippet: BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.

    Techniques Used: Inhibition

    BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.

    Techniques Used: Inhibition

    p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.
    Figure Legend Snippet: p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.

    Techniques Used: Inhibition, Transmission Assay, Activity Assay, Mouse Assay

    26) Product Images from "ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses"

    Article Title: ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2022.866802

    BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.

    Techniques Used: Concentration Assay, Inhibition

    BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.
    Figure Legend Snippet: BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.

    Techniques Used: Inhibition

    BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.

    Techniques Used: Inhibition

    p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.
    Figure Legend Snippet: p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.

    Techniques Used: Inhibition, Transmission Assay, Activity Assay, Mouse Assay

    27) Product Images from "ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses"

    Article Title: ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2022.866802

    BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.

    Techniques Used: Concentration Assay, Inhibition

    BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.
    Figure Legend Snippet: BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.

    Techniques Used: Inhibition

    BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.

    Techniques Used: Inhibition

    p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.
    Figure Legend Snippet: p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.

    Techniques Used: Inhibition, Transmission Assay, Activity Assay, Mouse Assay

    28) Product Images from "ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses"

    Article Title: ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2022.866802

    BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.

    Techniques Used: Concentration Assay, Inhibition

    BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.
    Figure Legend Snippet: BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.

    Techniques Used: Inhibition

    BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.

    Techniques Used: Inhibition

    p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.
    Figure Legend Snippet: p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.

    Techniques Used: Inhibition, Transmission Assay, Activity Assay, Mouse Assay

    29) Product Images from "ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses"

    Article Title: ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2022.866802

    BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.

    Techniques Used: Concentration Assay, Inhibition

    BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.
    Figure Legend Snippet: BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.

    Techniques Used: Inhibition

    BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.

    Techniques Used: Inhibition

    p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.
    Figure Legend Snippet: p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.

    Techniques Used: Inhibition, Transmission Assay, Activity Assay, Mouse Assay

    30) Product Images from "ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses"

    Article Title: ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2022.866802

    BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.

    Techniques Used: Concentration Assay, Inhibition

    BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.
    Figure Legend Snippet: BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.

    Techniques Used: Inhibition

    BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.

    Techniques Used: Inhibition

    p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.
    Figure Legend Snippet: p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.

    Techniques Used: Inhibition, Transmission Assay, Activity Assay, Mouse Assay

    31) Product Images from "ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses"

    Article Title: ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2022.866802

    BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.

    Techniques Used: Concentration Assay, Inhibition

    BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.
    Figure Legend Snippet: BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.

    Techniques Used: Inhibition

    BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.

    Techniques Used: Inhibition

    p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.
    Figure Legend Snippet: p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.

    Techniques Used: Inhibition, Transmission Assay, Activity Assay, Mouse Assay

    32) Product Images from "ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses"

    Article Title: ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2022.866802

    BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.

    Techniques Used: Concentration Assay, Inhibition

    BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.
    Figure Legend Snippet: BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.

    Techniques Used: Inhibition

    BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.

    Techniques Used: Inhibition

    p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.
    Figure Legend Snippet: p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.

    Techniques Used: Inhibition, Transmission Assay, Activity Assay, Mouse Assay

    33) Product Images from "ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses"

    Article Title: ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2022.866802

    BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.

    Techniques Used: Concentration Assay, Inhibition

    BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.
    Figure Legend Snippet: BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.

    Techniques Used: Inhibition

    BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.

    Techniques Used: Inhibition

    p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.
    Figure Legend Snippet: p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.

    Techniques Used: Inhibition, Transmission Assay, Activity Assay, Mouse Assay

    34) Product Images from "ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses"

    Article Title: ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2022.866802

    BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.

    Techniques Used: Concentration Assay, Inhibition

    BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.
    Figure Legend Snippet: BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.

    Techniques Used: Inhibition

    BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.
    Figure Legend Snippet: BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.

    Techniques Used: Inhibition

    p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.
    Figure Legend Snippet: p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.

    Techniques Used: Inhibition, Transmission Assay, Activity Assay, Mouse Assay

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    Alomone Labs bdnf prodomain
    <t>BDNF</t> <t>prodomain</t> in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.
    Bdnf Prodomain, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Alomone Labs recombinant rat ngf
    <t>TGF-β1</t> promoted the mRNA expression of <t>NGF</t> in SCDC2 cells through its type I receptor in a dose-dependent manner. After 24-h culture in growth medium, SCDC2 cells were starved for 24 h. The starved cells were then treated with (A) TGF-β1 at various concentrations for 24 h, or (B) pretreated with or without TGF-β type I receptor inhibitor SB-431542 (10 µ M) for 30 min and then with or without TGF-β1 (10 ng/ml) for 24 h. (C) Starved cells were treated with or without TGF-β1 (10 ng/ml) for the indicated times. The relative expression level of NGF was evaluated using reverse transcription-quantitative polymerase chain reaction. Data represent the mean ± standard deviation (n=6). * P
    Recombinant Rat Ngf, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Alomone Labs nerve growth factor ngf
    <t>BDNF-induced</t> NR2C upregulation by TrkB activation. Cells were cultured in low KCl and treated with or without BDNF (100 ng/ml in A and 50 ng/ml in B-D and F ) for 96 h. A , Levels of indicated mRNAs were quantitated by RNA blotting ( n = 4). B , Cell lysates (40 μg) were immunoblotted with anti-panNR2 antibody or anti-NR1 antibody. Molecular sizes (kilodaltons) of protein makers are indicated on the left. C , P2 membrane fractions were isolated, solubilized, and immunoprecipitated (IP) with anti-NR1 antibody, followed by immnoblotting with anti-panNR2 antibody. D , Cell-surface proteins were biotinylated with Sulfo-NHS-SS-Biotin. Cell lysates were solubilized, precipitated with NeutrAvidin beads, and immunoblotted with anti-panNR2 antibody. E , Cells were cultured in low KCl and treated with BDNF, <t>NGF,</t> NT-3, or NT-4 (50 ng/ml each) for 96 h. Levels of NR2C mRNA were quantitated ( n = 4). F , Granule cells were prepared from TrkB - / - knock-out mice(KO) and their wild-type (WT) littermates. NR2C and TrkB mRNAs were analyzed by RNA blotting. Ethidium bromide-stained 18s rRNA is also indicated. * p
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    BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.

    Journal: Frontiers in Cellular Neuroscience

    Article Title: ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses

    doi: 10.3389/fncel.2022.866802

    Figure Lengend Snippet: BDNF prodomain in low concentration (1 nM) pre-synaptically increases ACh quantal size and simultaneously induces oppositely directed presynaptic effects affecting the evoked ACh release at newly formed NMJs of reinnervated mouse m. EDL. (A) Representative recordings of MEPPs (left above) and mean MEPP amplitude and cumulative probability plots (right above), frequency and time-course parameters (left to right below) in control ( n = 20) and upon application of BDNF prodomain ( n = 22). (B) Mean MEPP amplitude in control ( n = 16) and during inhibition of vesicular ACh transporter by vesamicol (1 μM, n = 17) (left) and mean MEPP amplitude and cumulative probability plots in control ( n = 15) and upon application of BDNF prodomain in the presence of vesamicol ( n = 16). (C) Changes in the EPP amplitude (left) and their quantal content (right) in control ( n = 31) and in the presence of BDNF prodomain ( n = 41). Inset shows MEPP amplitudes.

    Article Snippet: Next, it was necessary to reveal which targets and signaling pathways mediate the negative effect of the BDNF prodomain on synaptic transmission in mature NMJs.

    Techniques: Concentration Assay, Inhibition

    BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.

    Journal: Frontiers in Cellular Neuroscience

    Article Title: ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses

    doi: 10.3389/fncel.2022.866802

    Figure Lengend Snippet: BK channels do not but GIRK channels mediate BDNF prodomain-induced inhibition of evoked ACh release at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of BK-blocker iberiotoxin (ITx, 100 nM) with L-type Ca 2+ -channel blocker nitrendipine (Nitr., 1 μM) ( n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and in the presence of GIRK blocker tertiapin-Q (100 nM, n = 17). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 16) and upon BDNF prodomain (1 nM) in the presence of tertiapin-Q ( n = 19). Insets show MEPP amplitudes.

    Article Snippet: Next, it was necessary to reveal which targets and signaling pathways mediate the negative effect of the BDNF prodomain on synaptic transmission in mature NMJs.

    Techniques: Inhibition

    BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.

    Journal: Frontiers in Cellular Neuroscience

    Article Title: ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses

    doi: 10.3389/fncel.2022.866802

    Figure Lengend Snippet: BDNF prodomain (1 nM) but not proBDNF (1 nM), induces strong inhibition of spontaneous end evoked ACh release at mature NMJs. (A) Mean MEPP amplitude, cumulative probability plots, frequency, and time-course parameters (left to right) in control ( n = 19) and upon application of proBDNF ( n = 26). (B) Representative recordings of MEPPs (top left) and mean MEPP amplitude, cumulative probability plots, frequency, (top right) and their time-course parameters (bottom) in control ( n = 23) and upon application of BDNF prodomain ( n = 33). (C) Representative recordings of EPPs during a short (1 s) high-frequency (50 Hz) train in control (above) and upon application of BDNF prodomain (below). (D) Changes in the EPP amplitude (above) and in the quantal content of EPPs (below) in control ( n = 22) and in the presence of proBDNF ( n = 21). Inset shows MEPP amplitudes.

    Article Snippet: Next, it was necessary to reveal which targets and signaling pathways mediate the negative effect of the BDNF prodomain on synaptic transmission in mature NMJs.

    Techniques: Inhibition

    p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.

    Journal: Frontiers in Cellular Neuroscience

    Article Title: ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses

    doi: 10.3389/fncel.2022.866802

    Figure Lengend Snippet: p75 receptors and Rho-signaling pathway underlie BDNF prodomain-triggered inhibition of evoked ACh release at mature NMJs. Moreover, the inhibitory effect of the BDNF prodomain (1 nM) on the evoked neuromuscular transmission depends on the endogenous activity of synaptic purinoreceptors at mature NMJs. (A) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 20) and upon BDNF prodomain (1 nM) in the presence of Rho-GDI-associated p75 signaling inhibitor TAT-Pep5 (1 μM, n = 21). (B) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 17) and in the presence of ROCK inhibitor Y-27632 (3 μM, n = 21). (C) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right) in control ( n = 15) and upon BDNF prodomain (1 nM) in the presence of Y-27632 ( n = 21). (D) Changes in the EPP amplitude (left) and in the quantal content of EPPs (right), registered from NMJs of Panx1 –/– mice in control ( n = 24) and in the presence of BDNF prodomain ( n = 22). Insets show MEPP amplitudes.

    Article Snippet: Next, it was necessary to reveal which targets and signaling pathways mediate the negative effect of the BDNF prodomain on synaptic transmission in mature NMJs.

    Techniques: Inhibition, Transmission Assay, Activity Assay, Mouse Assay

    TGF-β1 promoted the mRNA expression of NGF in SCDC2 cells through its type I receptor in a dose-dependent manner. After 24-h culture in growth medium, SCDC2 cells were starved for 24 h. The starved cells were then treated with (A) TGF-β1 at various concentrations for 24 h, or (B) pretreated with or without TGF-β type I receptor inhibitor SB-431542 (10 µ M) for 30 min and then with or without TGF-β1 (10 ng/ml) for 24 h. (C) Starved cells were treated with or without TGF-β1 (10 ng/ml) for the indicated times. The relative expression level of NGF was evaluated using reverse transcription-quantitative polymerase chain reaction. Data represent the mean ± standard deviation (n=6). * P

    Journal: International Journal of Molecular Medicine

    Article Title: IL-1β and TNF-α suppress TGF-β-promoted NGF expression in periodontal ligament-derived fibroblasts through inactivation of TGF-β-induced Smad2/3- and p38 MAPK-mediated signals

    doi: 10.3892/ijmm_2018.3714

    Figure Lengend Snippet: TGF-β1 promoted the mRNA expression of NGF in SCDC2 cells through its type I receptor in a dose-dependent manner. After 24-h culture in growth medium, SCDC2 cells were starved for 24 h. The starved cells were then treated with (A) TGF-β1 at various concentrations for 24 h, or (B) pretreated with or without TGF-β type I receptor inhibitor SB-431542 (10 µ M) for 30 min and then with or without TGF-β1 (10 ng/ml) for 24 h. (C) Starved cells were treated with or without TGF-β1 (10 ng/ml) for the indicated times. The relative expression level of NGF was evaluated using reverse transcription-quantitative polymerase chain reaction. Data represent the mean ± standard deviation (n=6). * P

    Article Snippet: Recombinant human TGF-β1 was obtained from PeproTech, Inc. (Rocky Hill, NJ, USA), recombinant rat NGF was obtained from Alomone Labs (Jerusalem, Israel), and recombinant rat IL-1β and TNF-α were purchased from Miltenyi Biotec GmbH (Bergisch Gladbach, Germany).

    Techniques: Expressing, Real-time Polymerase Chain Reaction, Standard Deviation

    IL-1β and TNF-α suppressed the TGF-β1-induced mRNA expression of NGF in SCDC2 cells by abrogating Smad2/3 and p38 MAPK activities. The effects of IL-1β and TNF-α on TGF-β1-induced mRNA expression of NGF in SCDC2 cells were evaluated using RT-qPCR. The cells were treated with or without (A) IL-1β alone or (B) TNF-α alone at indicated concentrations, (C) TGF-β1 (10 ng/ml) and/or IL-1β (10 ng/ml), and (D) TGF-β1 (10 ng/ml) and/or TNF-α (10 ng/ml). Data represent the mean ± standard deviation (n=6). * P

    Journal: International Journal of Molecular Medicine

    Article Title: IL-1β and TNF-α suppress TGF-β-promoted NGF expression in periodontal ligament-derived fibroblasts through inactivation of TGF-β-induced Smad2/3- and p38 MAPK-mediated signals

    doi: 10.3892/ijmm_2018.3714

    Figure Lengend Snippet: IL-1β and TNF-α suppressed the TGF-β1-induced mRNA expression of NGF in SCDC2 cells by abrogating Smad2/3 and p38 MAPK activities. The effects of IL-1β and TNF-α on TGF-β1-induced mRNA expression of NGF in SCDC2 cells were evaluated using RT-qPCR. The cells were treated with or without (A) IL-1β alone or (B) TNF-α alone at indicated concentrations, (C) TGF-β1 (10 ng/ml) and/or IL-1β (10 ng/ml), and (D) TGF-β1 (10 ng/ml) and/or TNF-α (10 ng/ml). Data represent the mean ± standard deviation (n=6). * P

    Article Snippet: Recombinant human TGF-β1 was obtained from PeproTech, Inc. (Rocky Hill, NJ, USA), recombinant rat NGF was obtained from Alomone Labs (Jerusalem, Israel), and recombinant rat IL-1β and TNF-α were purchased from Miltenyi Biotec GmbH (Bergisch Gladbach, Germany).

    Techniques: Expressing, Quantitative RT-PCR, Standard Deviation

    TGF-β1 promoted the mRNA expression of NGF in SCDC2 cells in Smad2/3-dependent and p38 MAPK-dependent manners. Effects of (A) SIS3 (10 µ M), and (B) SB203580 (10 µ M) on expression of NGF mRNA were evaluated as described in Materials and methods. Data represent the mean ± standard deviation (n=6). * P

    Journal: International Journal of Molecular Medicine

    Article Title: IL-1β and TNF-α suppress TGF-β-promoted NGF expression in periodontal ligament-derived fibroblasts through inactivation of TGF-β-induced Smad2/3- and p38 MAPK-mediated signals

    doi: 10.3892/ijmm_2018.3714

    Figure Lengend Snippet: TGF-β1 promoted the mRNA expression of NGF in SCDC2 cells in Smad2/3-dependent and p38 MAPK-dependent manners. Effects of (A) SIS3 (10 µ M), and (B) SB203580 (10 µ M) on expression of NGF mRNA were evaluated as described in Materials and methods. Data represent the mean ± standard deviation (n=6). * P

    Article Snippet: Recombinant human TGF-β1 was obtained from PeproTech, Inc. (Rocky Hill, NJ, USA), recombinant rat NGF was obtained from Alomone Labs (Jerusalem, Israel), and recombinant rat IL-1β and TNF-α were purchased from Miltenyi Biotec GmbH (Bergisch Gladbach, Germany).

    Techniques: Expressing, Standard Deviation

    BDNF-induced NR2C upregulation by TrkB activation. Cells were cultured in low KCl and treated with or without BDNF (100 ng/ml in A and 50 ng/ml in B-D and F ) for 96 h. A , Levels of indicated mRNAs were quantitated by RNA blotting ( n = 4). B , Cell lysates (40 μg) were immunoblotted with anti-panNR2 antibody or anti-NR1 antibody. Molecular sizes (kilodaltons) of protein makers are indicated on the left. C , P2 membrane fractions were isolated, solubilized, and immunoprecipitated (IP) with anti-NR1 antibody, followed by immnoblotting with anti-panNR2 antibody. D , Cell-surface proteins were biotinylated with Sulfo-NHS-SS-Biotin. Cell lysates were solubilized, precipitated with NeutrAvidin beads, and immunoblotted with anti-panNR2 antibody. E , Cells were cultured in low KCl and treated with BDNF, NGF, NT-3, or NT-4 (50 ng/ml each) for 96 h. Levels of NR2C mRNA were quantitated ( n = 4). F , Granule cells were prepared from TrkB - / - knock-out mice(KO) and their wild-type (WT) littermates. NR2C and TrkB mRNAs were analyzed by RNA blotting. Ethidium bromide-stained 18s rRNA is also indicated. * p

    Journal: The Journal of Neuroscience

    Article Title: Neuronal Depolarization Controls Brain-Derived Neurotrophic Factor-Induced Upregulation of NR2C NMDA Receptor via Calcineurin Signaling

    doi: 10.1523/JNEUROSCI.2191-05.2005

    Figure Lengend Snippet: BDNF-induced NR2C upregulation by TrkB activation. Cells were cultured in low KCl and treated with or without BDNF (100 ng/ml in A and 50 ng/ml in B-D and F ) for 96 h. A , Levels of indicated mRNAs were quantitated by RNA blotting ( n = 4). B , Cell lysates (40 μg) were immunoblotted with anti-panNR2 antibody or anti-NR1 antibody. Molecular sizes (kilodaltons) of protein makers are indicated on the left. C , P2 membrane fractions were isolated, solubilized, and immunoprecipitated (IP) with anti-NR1 antibody, followed by immnoblotting with anti-panNR2 antibody. D , Cell-surface proteins were biotinylated with Sulfo-NHS-SS-Biotin. Cell lysates were solubilized, precipitated with NeutrAvidin beads, and immunoblotted with anti-panNR2 antibody. E , Cells were cultured in low KCl and treated with BDNF, NGF, NT-3, or NT-4 (50 ng/ml each) for 96 h. Levels of NR2C mRNA were quantitated ( n = 4). F , Granule cells were prepared from TrkB - / - knock-out mice(KO) and their wild-type (WT) littermates. NR2C and TrkB mRNAs were analyzed by RNA blotting. Ethidium bromide-stained 18s rRNA is also indicated. * p

    Article Snippet: Slices were treated with or without 1 μ m FK506 for 96 h, and 0.5 vol of the culture medium was changed every 2 d. Reagents and inhibitors were purchased from the following sources: BDNF (Peprotech, London, UK); neurotrophin-3 (NT-3), NT-4, and nerve growth factor (NGF) (Alomone Laboratories, Jerusalem, Israel); neuregulin-β (NeoMarkers, Fremont, CA); nifedipine (Nacalai Tesque, Kyoto, Japan); KN62 (Tocris, Bristol, UK); and U0126, SB203580, FK506, K252a, , PD98059, cyclosporin A, rapamycin, and bisindolylmaleimide I (Calbiochem, San Diego, CA).

    Techniques: Activation Assay, Cell Culture, Isolation, Immunoprecipitation, Knock-Out, Mouse Assay, Staining