Interactions Between Asynchronous Release and Short-Term Plasticity in the Nucleus Accumbens Slice

2006 ◽  
Vol 95 (3) ◽  
pp. 2020-2023 ◽  
Author(s):  
Gregory O. Hjelmstad
Keyword(s):  
Nucleus Accumbens ◽  
Synaptic Transmission ◽  
Short Term ◽  
Short Term Plasticity ◽  
Releasable Pool ◽  
Readily Releasable Pool ◽  
Glutamate Synapses ◽  
Asynchronous Release

Glutamate synapses in the nucleus accumbens (NAc) display asynchronous release in response to trains of stimulation. However, it is unclear what role this asynchronous release plays in synaptic transmission in this nucleus. This process was studied, specifically looking at the interaction between short-term depression and asynchronous release. These results indicate that synchronous and asynchronous release do not compete for a depleted readily releasable pool of vesicles.

A Simple Depletion Model of the Readily Releasable Pool of Synaptic Vesicles Cannot Account for Paired-Pulse Depression

2007 ◽  
Vol 97 (1) ◽  
pp. 948-950 ◽  
Author(s):  
Jane M. Sullivan
Keyword(s):  
Synaptic Vesicles ◽  
Hippocampal Neurons ◽  
Synaptic Activity ◽  
Excitatory Synapses ◽  
Short Term ◽  
Paired Pulse ◽  
Short Term Plasticity ◽  
Releasable Pool ◽  
Readily Releasable Pool ◽  
Paired Pulse Depression

Paired-pulse depression (PPD) is a form of short-term plasticity that plays a central role in processing of synaptic activity and is manifest as a decrease in the size of the response to the second of two closely timed stimuli. Despite mounting evidence to the contrary, PPD is still commonly thought to reflect depletion of the pool of synaptic vesicles available for release in response to the second stimulus. Here it is shown that PPD cannot be accounted for by depletion at excitatory synapses made by hippocampal neurons because PPD is unaffected by changes in the fraction of the readily releasable pool (RRP) released by the first of a pair of pulses.

scholarly journals Doc2-mediated superpriming supports synaptic augmentation

2018 ◽  
Vol 115 (24) ◽  
pp. E5605-E5613 ◽  
Author(s):  
Renhao Xue ◽  
David A. Ruhl ◽  
Joseph S. Briguglio ◽  
Alexander G. Figueroa ◽  
Robert A. Pearce ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Synaptic Plasticity ◽  
Learning And Memory ◽  
Synaptic Vesicles ◽  
Hippocampal Neurons ◽  
Underlying Mechanism ◽  
Short Term ◽  
Short Term Plasticity ◽  
Releasable Pool ◽  
Readily Releasable Pool

Various forms of synaptic plasticity underlie aspects of learning and memory. Synaptic augmentation is a form of short-term plasticity characterized by synaptic enhancement that persists for seconds following specific patterns of stimulation. The mechanisms underlying this form of plasticity are unclear but are thought to involve residual presynaptic Ca2+. Here, we report that augmentation was reduced in cultured mouse hippocampal neurons lacking the Ca2+ sensor, Doc2; other forms of short-term enhancement were unaffected. Doc2 binds Ca2+ and munc13 and translocates to the plasma membrane to drive augmentation. The underlying mechanism was not associated with changes in readily releasable pool size or Ca2+ dynamics, but rather resulted from superpriming a subset of synaptic vesicles. Hence, Doc2 forms part of the Ca2+-sensing apparatus for synaptic augmentation via a mechanism that is molecularly distinct from other forms of short-term plasticity.

scholarly journals A General Model of Synaptic Transmission and Short-Term Plasticity

Neuron ◽  
2009 ◽  
Vol 62 (4) ◽  
pp. 539-554 ◽  
Author(s):  
Bin Pan ◽  
Robert S. Zucker
Keyword(s):  
Synaptic Transmission ◽  
General Model ◽  
Short Term ◽  
Short Term Plasticity

scholarly journals Ca2+/Calmodulin and Presynaptic Short-Term Plasticity

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Sumiko Mochida
Keyword(s):  
Transmitter Release ◽  
Presynaptic Terminal ◽  
Neuronal Firing ◽  
Firing Activity ◽  
Short Term ◽  
Short Term Plasticity ◽  
Readily Releasable Pool ◽  
Ef Hand ◽  
Sensor Protein ◽  
Activity Dependent

Synaptic efficacy is remodeled by neuronal firing activity at the presynaptic terminal. Presynaptic activity-dependent changes in transmitter release induce postsynaptic plasticity, including morphological change in spine, gene transcription, and protein synthesis and trafficking. The presynaptic transmitter release is triggered and regulated by Ca2+, which enters through voltage-gated Ca2+ (CaV) channels and diffuses into the presynaptic terminal accompanying action potential firings. Residual Ca2+ is sensed by Ca2+-binding proteins, among other potential actions, it mediates time- and space-dependent synaptic facilitation and depression via effects on CaV2 channel gating and vesicle replenishment in the readily releasable pool (RRP). Calmodulin, a Ca2+-sensor protein with an EF-hand motif that binds Ca2+, interacts with CaV2 channels and autoreceptors in modulation of SNARE-mediated exocytosis.

Synaptic transmission and short-term plasticity at the calyx of Held synapse revealed by multielectrode array recordings

2008 ◽  
Vol 174 (2) ◽  
pp. 227-236 ◽  
Author(s):  
Martin D. Haustein ◽  
Thomas Reinert ◽  
Annika Warnatsch ◽  
Bernhard Englitz ◽  
Beatrice Dietz ◽  
...  
Keyword(s):  
Synaptic Transmission ◽  
Multielectrode Array ◽  
Short Term ◽  
Calyx Of Held ◽  
Short Term Plasticity ◽  
Array Recordings

Pre- and Post-Synaptically Induced Short-Term Plasticity of GABA-ergic Synaptic Transmission

2005 ◽  
Vol 37 (3) ◽  
pp. 261-272 ◽  
Author(s):  
M. V. Storozhuk ◽  
S. Yu. Ivanova ◽  
P. G. Kostyuk
Keyword(s):  
Synaptic Transmission ◽  
Short Term ◽  
Short Term Plasticity

scholarly journals Reexamination of N-terminal domains of Syntaxin-1 in vesicle fusion from central murine synapses

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Gülçin Vardar ◽  
Andrea Salazar-Lázaro ◽  
Marisa M Brockmann ◽  
Marion Weber-Boyvat ◽  
Sina Zobel ◽  
...  
Keyword(s):  
Synaptic Transmission ◽  
Neurotransmitter Release ◽  
Null Mouse ◽  
General View ◽  
Binding Modes ◽  
Short Term ◽  
Short Term Plasticity ◽  
Open Conformation ◽  
Vesicular Release ◽  
Mouse Model System

Syntaxin-1 (STX1) and Munc18-1 are two requisite components of synaptic vesicular release machinery, so much so synaptic transmission cannot proceed in their absence. They form a tight complex through two major binding modes: through STX1's N-peptide and through STX's closed conformation driven by its Habc- domain. However, physiological roles of these two reportedly different binding modes in synapses are still controversial. Here we characterized the roles of STX1's N-peptide, Habc-domain, and open conformation with and without N-peptide deletion using our STX1-null mouse model system and exogenous reintroduction of STX1A mutants. We show, on the contrary to the general view, that the Habc-domain is absolutely required and N-peptide is dispensable for synaptic transmission. However, STX1A's N-peptide plays a regulatory role, particularly in the Ca2+-sensitivity and the short-term plasticity of vesicular release, whereas STX1's open-conformation governs the vesicle fusogenicity. Strikingly, we also show neurotransmitter release still proceeds when the two interaction modes between STX1A and Munc18-1 are presumably intervened, necessitating a refinement of the conceptualization of STX1A-Munc18-1 interaction.

Augmentation Controls the Fast Rebound From Depression at Excitatory Hippocampal Synapses

2008 ◽  
Vol 99 (4) ◽  
pp. 1770-1786 ◽  
Author(s):  
Elizabeth Garcia-Perez ◽  
John F. Wesseling
Keyword(s):  
Neurotransmitter Release ◽  
Single Pulse ◽  
Maximal Level ◽  
Short Term ◽  
Paired Pulse ◽  
Short Term Plasticity ◽  
Readily Releasable Pool ◽  
Hippocampal Synapses ◽  
Low Probability ◽  
Chemical Synapses

Short-term plasticity occurs at most central chemical synapses and includes both positive and negative components, but the principles governing interaction between components are largely unknown. The residual Ca2+ that persists in presynaptic terminals for several seconds after repetitive use is known to enhance neurotransmitter release under artificial, low probability of release conditions where depression is absent; this is termed augmentation. However, the full impact of augmentation under standard conditions at synapses where depression dominates is not known because of possibly complicated convolution with a variety of potential depression mechanisms. This report shows that residual Ca2+ continues to have a large enhancing impact on release at excitatory hippocampal synapses recovering from depression, including when only recently recruited vesicles are available for release. No evidence was found for gradual vesicle priming or for fast refilling of a highly releasable subdivision of the readily releasable pool (RRP). And decay of enhancement matched the clearance of residual Ca2+, thus matching the behavior of augmentation when studied in isolation. Because of incomplete RRP replenishment, synaptic strength was not typically increased above baseline when residual Ca2+ levels were highest. Instead residual Ca2+ caused single pulse release probability to rebound quickly from depression and then depress quickly during subsequent bursts of activity. Together, these observations can help resolve discrepancies in recent timing estimates of recovery from depression. Additionally, in contrast to results obtained under reduced release conditions, augmentation could be driven to a maximal level, occluding paired-pulse facilitation and other mechanisms that increase release efficiency.

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