bdnf prodomain (Alomone Labs)
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bdnf prodomain
Bdnf Prodomain, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 97/100, based on 34 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/bdnf prodomain/product/Alomone Labs
Average 97 stars, based on 34 article reviews
Price from $9.99 to $1999.99
Bdnf Prodomain, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 97/100, based on 34 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/bdnf prodomain/product/Alomone Labs
Average 97 stars, based on 34 article reviews
Price from $9.99 to $1999.99
bdnf prodomain - by Bioz Stars,
2022-08
97/100 stars
Images
1) Product Images from "ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses"
Article Title: ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses
Journal: Frontiers in Cellular Neuroscience
doi: 10.3389/fncel.2022.866802
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 "Astrocytic microdomains from mouse cortex gain molecular control over long-term information storage and memory retention"
Article Title: Astrocytic microdomains from mouse cortex gain molecular control over long-term information storage and memory retention
Journal: Communications Biology
doi: 10.1038/s42003-021-02678-x
Figure Legend Snippet: astrocytic BDNFpro secretion rescues LTP deficit in p75-flox mice. a Schematic representation of the experimental design. Step I, deletion of p75 NTR in astrocytes from tamoxifen-treated p75-flox mice precludes proBDNF transfer from neurons to astrocyte following TBS. Step II, LV-BDNFpro stop transduction replaces BDNFpro in astrocytes. Schematic representation of the experimental paradigms (right); mice were treated with tamoxifen (−5 to 0), injected with lentiviruses the last day of tamoxifen treatment (0 dptm) and finally recorded (14 dptm). LTP evoked in slices from p75-flox mice and control littermates injected with LV-GFP stop or LV-BDNFpro stop is shown. *** p
Techniques Used: Mouse Assay, Transduction, Injection
Figure Legend Snippet: BDNFpro restores memory retention in p75-flox mice. a Schematic diagram depicting the behavioral paradigm used for ORT. Mice were subjected to familiarization (sample phase) with two identical objects (circles). A test phase in which one familiar object (circle) is substituted with a novel one was performed after 10 min (square) and 24 h (triangle). b Schematic diagram depicting the experimental paradigm. p75-flox mice and control littermates treated with tamoxifen (−5 to 0) and injected with LV-GFP stop or LV-BDNFpro stop the last day of tamoxifen treatment (0 dptm) were subjected to ORT (14 dptm). Discrimination index is plotted against time interval between sample phase and test phases. ** p
Techniques Used: Mouse Assay, Injection
Figure Legend Snippet: post-synaptic targeting of TrkB/SorCS2 complex. a Schematic representation of the experimental design. Circular DNA probes (−) and (+) are coupled to II° antibody targeting αSorCS2 and αTrkB I° antibody. BDNFpro induces TrkB/SorCS2 complex formation (PLA TrkB/SorCS2 ) that is prevented in the presence of αSorCS2 (blocking) antibody. b Panels show PLA TrkB/SorCS2 signals in primary culture of cortical neurons treated with vehicle or BDNFpro. The insets show reference GFP-neurons. Scale bars: 5 μm. c Panels show a GFP-neuron treated with BDNFpro. Scale bar: 5 μm. Magnification of regions of interest 1 and 2 shows dendritic PLA TrkB/SorCS2 localization (red arrowheads). Scale bar: 1 μm. d Quantification of PLA TrkB/SorCS2 signal in cultured neurons treated with vehicle, BDNFpro (in presence or absence of αSorCS2), mBDNF or proBDNF CR . Data are presented as mean ± SEM; ** p
Techniques Used: Proximity Ligation Assay, Blocking Assay, Cell Culture
Figure Legend Snippet: BDNFpro-induced TrkB/SorCS2 targeting. a Schematic representation of the experimental design. Step I, deletion of p75 NTR in astrocytes from tamoxifen-treated p75-flox mice precludes proBDNF transfer from neurons to astrocyte following TBS. Step II, LV-BDNFpro stop transduction replaces BDNFpro in astrocytes. Step III, astrocytic BDNFpro provides final increase of TrkB/SorCS2 complexes in dendritic spines and LTP maintenance. b z-stack reconstruction showing NeuN/PLA TrkB/SorCS2 colocalization signal in TBS-slices from p75-flox mice transduced with LV-GFP stop or LV-BDNFpro stop . Scale bars: 40 μm. The insets show the field of analysis. Scale bars: 15 μm. NeuN/PLA TrkB/SorCS2 colocalization was quantified using Mander’s overlap. ** p
Techniques Used: Mouse Assay, Transduction, Proximity Ligation Assay
Figure Legend Snippet: BDNFpro expression in cortical astrocytes. a Schematic representation of proBDNF precursor and cleaved BDNFpro domain. αBDNFpro antibody recognizes the furin cleavage site of the prodomain. Western blotting probing recombinant mBDNF, BDNFpro, and proBDNF CR with αBDNFpro and αmBDNF antibodies. b Cortical slices from control mice injected with AAV-GFAP-GFP virus were recorded and fixed 10 min after TBS for immunostaining. z-stack reconstruction shows astrocytes labeled by GFP. Magnification of a single stack from a region of interest (ROI) shows BDNFpro immunoreactivity and BDNFpro/GFP colocalization signal of one GFP-astrocyte delimited by an approximate territory (white dashed). Scale bars: 10 µm. c z-stack reconstruction of BDNFpro/GFP colocalization signals in astrocytes from baseline- and TBS-slices from control mice. The insets show GFP signal. BDNFpro/GFP colocalization was quantified in the whole cell and branches using Mander’s overlap. *** p
Techniques Used: Expressing, Western Blot, Recombinant, Mouse Assay, Injection, Immunostaining, Labeling
Figure Legend Snippet: subcellular localization of BDNFpro. a Graphical representation of the SIM super-resolution microscope. 3D-SIM image of a GFP-labeled astrocyte in a TBS-slice from control mice. Scale bar: 10 µm. Magnification of a ROI shows BDNFpro/GFP colocalization signal localized in fine membrane extensions of the cell periphery. Scale bar: 200 nm. b 3D-SIM image of the ROI in ( a ); z-axe is visualized in pseudocolor to facilitate microdomains identification. Scale bar: 200 nm. Magnification of microdomains characterized by the typical fingerlike extension (dashed squares 1 and 2) and flat lamellar sheath (dashed squares 3 and 4) are shown. BDNFpro/GFP colocalization is indicated (red arrowheads). Scale bars: 40 nm.
Techniques Used: Microscopy, Labeling, Mouse Assay
Figure Legend Snippet: vesicular localization of BDNFpro. a z-stack reconstruction shows astrocytes labeled by GFP. Cortical slices from control mice injected with AAV-GFAP-GFP virus were fixed 10 min after TBS and processed for immunostaining and confocal analysis. Scale bar: 10 µm. Magnification of a ROI shows one GFP-astrocyte delimited by an approximate territory (white dashed). Scale bar: 10 µm. BDNFpro/GFP and Vamp2/GFP co-localizations signals are shown. Magnification shows representative areas (dashed squares 1 to 4) in which BDNFpro/GFP and Vamp2/GFP signals overlap. Scale bars: 1 µm. b 3D-SIM image of a GFP-labeled astrocyte in a TBS-slice from control mice. Scale bar: 10 µm. Magnification of a ROI shows BDNFpro/Vamp2 colocalization signal. Scale bar: 500 nm. Magnification shows BDNFpro/Vamp2 colocalization signal in fine membrane extensions of the cell periphery (dashed squares 1 to 4). Scale bars: 50 nm. c EM image depicts BDNFpro-gold at astrocytic microdomains (light blue) surrounding an axon bouton. Scale bar: 100 nm. Magnification of the ROI shows gold particles (red arrowheads) in vesicular-like structures. Scale bar: 20 nm. d Digital reconstruction of the image in ( c ). Astrocytic vesicles (black boundary) are shown.
Techniques Used: Labeling, Mouse Assay, Injection, Immunostaining
Figure Legend Snippet: localization of BDNFpro in astrocytic microdomains. a Experimental design linking field-potential with electron microscopy (EM) in layer II/III perirhinal cortex. TBS (10 min)-slices were dissected for EM processing. b Representative EM-image depicts BDNFpro-gold particles at axon bouton (dashed squares 1 to 4) and dendritic spine (dashed squares 5 and 6). Scale bar: 100 nm. Magnification indicates representative areas (dashed squares 1 to 6) in which gold particles (red arrowheads) localization is shown. Scale bars: 10 nm. c Representative EM-image depicts BDNFpro-gold particles (dashed squares 1 to 6) at astrocytic microdomains (light blue) Scale bar: 250 nm. Magnification indicates representative areas (dashed squares 1 to 6) in which gold particles (red arrowheads) localization is shown. Scale bars: 20 nm. d Dot plot depicts the number of BDNFpro-gold particles in whole astrocytes and peri-synaptic astrocytes counted per section ( n = 41 sections, 5 slices, 3 mice). e Dot plot depicts the percentage of BDNFpro-gold particles at peri-synaptic astrocytes ( n = 41 sections, 5 slices, 3 mice). Data are mean ± SEM.
Techniques Used: Electron Microscopy, Mouse Assay
11) Product Images from "ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses"
Article Title: ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses
Journal: Frontiers in Cellular Neuroscience
doi: 10.3389/fncel.2022.866802
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 "Identification of a Linear Epitope in Sortilin That Partakes in Pro-neurotrophin Binding *"
Article Title: Identification of a Linear Epitope in Sortilin That Partakes in Pro-neurotrophin Binding *
Journal: The Journal of Biological Chemistry
doi: 10.1074/jbc.M109.062364
Figure Legend Snippet: Differential binding of pro-BDNF and neurotension to sortilin and pro-sortilin. A , SPR analysis showing that unprocessed pro-BDNF (50 n m ) binds nearly as efficiently to the receptor in the presence (pro-sortilin) as in the absence (sortilin) of the receptor
Techniques Used: Binding Assay, SPR Assay
Figure Legend Snippet: Selective competition of ligands by sortilin-derived peptide antagonist. SPR binding analysis of 50 n m unprocessed pro-BDNF ( A ), 50 n m unprocessed pro-NGF ( B ), and 90 n m RAP ( C ) to immobilized sortilin in the absence and presence of the sort166–181
Techniques Used: Derivative Assay, SPR Assay, Binding Assay
Figure Legend Snippet: Mutation of the linear binding site specifically impairs binding of both the NGF and the BDNF pro-domains. SPR analysis showing reduced binding of equal amounts (analyte concentration: 200 n m ) of the soluble extracellular domains of sortilin-4A compared
Techniques Used: Mutagenesis, Binding Assay, SPR Assay, Concentration Assay
21) Product Images from "ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses"
Article Title: ProBDNF and Brain-Derived Neurotrophic Factor Prodomain Differently Modulate Acetylcholine Release in Regenerating and Mature Mouse Motor Synapses
Journal: Frontiers in Cellular Neuroscience
doi: 10.3389/fncel.2022.866802
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
