scholarly journals The Core Membrane Fusion Complex Governs the Probability of Synaptic Vesicle Fusion But Not Transmitter Release Kinetics

2002 ◽  
Vol 22 (4) ◽  
pp. 1266-1272 ◽  
Author(s):  
Michael F. A. Finley ◽  
Sejal M. Patel ◽  
Daniel V. Madison ◽  
Richard H. Scheller
eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Vincent Huson ◽  
Marieke Meijer ◽  
Rien Dekker ◽  
Mirelle ter Veer ◽  
Marvin Ruiter ◽  
...  

Previously, we showed that modulation of the energy barrier for synaptic vesicle fusion boosts release rates supralinearly (Schotten, 2015). Here we show that mouse hippocampal synapses employ this principle to trigger Ca2+-dependent vesicle release and post-tetanic potentiation (PTP). We assess energy barrier changes by fitting release kinetics in response to hypertonic sucrose. Mimicking activation of the C2A domain of the Ca2+-sensor Synaptotagmin-1 (Syt1), by adding a positive charge (Syt1D232N) or increasing its hydrophobicity (Syt14W), lowers the energy barrier. Removing Syt1 or impairing its release inhibitory function (Syt19Pro) increases spontaneous release without affecting the fusion barrier. Both phorbol esters and tetanic stimulation potentiate synaptic strength, and lower the energy barrier equally well in the presence and absence of Syt1. We propose a model where tetanic stimulation activates Syt1-independent mechanisms that lower the energy barrier and act additively with Syt1-dependent mechanisms to produce PTP by exerting multiplicative effects on release rates.


2020 ◽  
Author(s):  
Vincent Huson ◽  
Marieke Meijer ◽  
Rien Dekker ◽  
Mirelle ter Veer ◽  
Marvin Ruiter ◽  
...  

AbstractPreviously, we showed that modulation of the energy barrier for synaptic vesicle fusion boosts release rates supralinearly (Schotten, 2015). Here we show that mouse hippocampal synapses employ this principle to trigger Ca2+-dependent vesicle release and post-tetanic potentiation (PTP). We assess energy barrier changes by fitting release kinetics in response to hypertonic sucrose. Mimicking activation of the C2A domain of the Ca2+-sensor Synaptotagmin-1 (Syt1), by adding a positive charge (Syt1D232N) or increasing its hydrophobicity (Syt14W), lowers the energy barrier. Removing Syt1 or impairing its release inhibitory function (Syt19Pro) increases spontaneous release without affecting the fusion barrier. Both phorbol esters and tetanic stimulation potentiate synaptic strength, and lower the energy barrier equally well in the presence and absence of Syt1. We propose a model where tetanic stimulation activates Syt1 dependent and independent mechanisms that lower the energy barrier independently in an additive manner to produce PTP by multiplication of release rates.


Neuron ◽  
1995 ◽  
Vol 14 (5) ◽  
pp. 991-998 ◽  
Author(s):  
Yun Kee ◽  
Richard C Lin ◽  
Shu-Chan Hsu ◽  
Richard H Scheller

PLoS ONE ◽  
2014 ◽  
Vol 9 (6) ◽  
pp. e100710 ◽  
Author(s):  
Guido A. Zampighi ◽  
Raul Serrano ◽  
Julio L. Vergara

2009 ◽  
Vol 110 (4) ◽  
pp. 1135-1149 ◽  
Author(s):  
Gerald R. Prescott ◽  
Oforiwa A. Gorleku ◽  
Jennifer Greaves ◽  
Luke H. Chamberlain

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