bdnf prodomain (Alomone Labs)


Structured Review

Bdnf Prodomain, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 97/100, based on 40 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 97 stars, based on 40 article reviews
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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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 "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

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

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

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

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
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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 "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

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

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

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

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
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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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
35) 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

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

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

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

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
36) 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

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

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

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

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
37) 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

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

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

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

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
38) 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

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

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

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

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
39) 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

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

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

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

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
40) 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

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

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

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

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