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

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.

Structural Contributions to Short-Term Synaptic Plasticity

2004 ◽  
Vol 84 (1) ◽  
pp. 69-85 ◽  
Author(s):  
MATTHEW A. XU-FRIEDMAN ◽  
WADE G. REGEHR
Keyword(s):  
Synaptic Plasticity ◽  
Synaptic Transmission ◽  
Synaptic Strength ◽  
Short Term ◽  
Ongoing Activity ◽  
Short Term Plasticity ◽  
Synaptic Ultrastructure

Xu-Friedman, Matthew A., and Wade G. Regehr. Structural Contributions to Short-Term Synaptic Plasticity. Physiol Rev 84: 69–85, 2004; 10.1152/physrev.00016.2003.—Synaptic ultrastructure is critical to many basic hypotheses about synaptic transmission. Various aspects of synaptic ultrastructure have also been implicated in the mechanisms of short-term plasticity. These forms of plasticity can greatly affect synaptic strength during ongoing activity. We review the evidence for how synaptic ultrastructure may contribute to facilitation, depletion, saturation, and desensitization.

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.

scholarly journals Towards biologically constrained attractor models of schizophrenia

2021 ◽  
Author(s):  
Heike Stein ◽  
Joao Barbosa ◽  
Albert Compte
Keyword(s):  
Working Memory ◽  
Synaptic Transmission ◽  
Firing Rate ◽  
Experimental Evidence ◽  
Cognitive Deficits ◽  
Critical Points ◽  
Network Models ◽  
Short Term ◽  
Short Term Plasticity ◽  
Network Simulations

Alterations in neuromodulation or synaptic transmission in biophysical attractor network models, as proposed by the dominant dopaminergic and glutamatergic theories of schizophrenia, successfully mimic working memory (WM) deficits in people with schizophrenia (PSZ). Yet, multiple, often opposing circuit mechanisms can lead to the same behavioral patterns in these network models. Here, we critically revise the computational and experimental literature that links NMDAR hypofunction to WM precision loss in PSZ. We show in network simulations that currently available experimental evidence cannot set apart competing mechanistic accounts, and critical points to resolve are firing rate tuning and shared noise modulations by E/I ratio alterations through NMDAR blockade, and possible concomitant deficits in short-term plasticity. We argue that these concerted experimental and computational efforts will lead to a better understanding of the neurobiology underlying cognitive deficits in PSZ.

scholarly journals Synaptic co-transmission of acetylcholine and GABA regulates hippocampal states

2017 ◽  
Author(s):  
Virág T. Takács ◽  
Csaba Cserép ◽  
Dániel Schlingloff ◽  
Balázs Pósfai ◽  
András Szőnyi ◽  
...  
Keyword(s):  
Synaptic Transmission ◽  
Neurodegenerative Disorders ◽  
Basal Forebrain ◽  
Cholinergic System ◽  
Epileptiform Activity ◽  
Short Term ◽  
Main Text ◽  
Short Term Plasticity ◽  
Synaptic Control ◽  
Novel Model

SummaryThe basal forebrain cholinergic system is widely assumed to control cortical functions via non-synaptic transmission of a single neurotransmitter, acetylcholine. Yet, using immune-electron tomographic, molecular anatomical, optogenetic and physiological techniques, we find that mouse hippocampal cholinergic terminals invariably establish synapses and their vesicles dock at synapses only. We demonstrate that these synapses do not co-release but co-transmit GABA and acetylcholine via different vesicles, whose release is triggered by distinct calcium channels. This co-transmission evokes fast composite postsynaptic potentials, which are mutually cross-regulated by presynaptic auto-receptors and display different short-term plasticity. The GABAergic component alone effectively suppresses hippocampal sharp wave-ripples and epileptiform activity. The synaptic nature of the forebrain cholinergic system with differentially regulated, fast, GABAergic and cholinergic co-transmission suggests a hitherto unrecognized level of synaptic control over cortical states. This novel model of hippocampal cholinergic neurotransmission could form the basis for alternative pharmacotherapies after cholinergic deinnervation seen in neurodegenerative disorders.Supplementary materials are attached after the main text.

scholarly journals Retinohypothalamic Tract Synapses in the Rat Suprachiasmatic Nucleus Demonstrate Short-Term Synaptic Plasticity

2010 ◽  
Vol 103 (5) ◽  
pp. 2390-2399 ◽  
Author(s):  
Mykhaylo G. Moldavan ◽  
Charles N. Allen
Keyword(s):  
Synaptic Transmission ◽  
Suprachiasmatic Nucleus ◽  
Ganglion Cells ◽  
Brain Slices ◽  
Release Mechanism ◽  
Dependent Manner ◽  
Short Term ◽  
Frequency Dependent ◽  
Short Term Plasticity ◽  
Retinohypothalamic Tract

The master circadian pacemaker located in the suprachiasmatic nucleus (SCN) is entrained by light intensity–dependent signals transmitted via the retinohypothalamic tract (RHT). Short-term plasticity at glutamatergic RHT–SCN synapses was studied using stimulus frequencies that simulated the firing of light sensitive retinal ganglion cells. The evoked excitatory postsynaptic current (eEPSC) was recorded from SCN neurons located in hypothalamic brain slices. The eEPSC amplitude was stable during 0.08 Hz stimulation and exhibited frequency-dependent short-term synaptic depression (SD) during 0.5 to 100 Hz stimulus trains in 95 of 99 (96%) recorded neurons. During SD the steady-state eEPSC amplitude decreased, whereas the cumulative charge transfer increased in a frequency-dependent manner and saturated at 20 Hz. SD was similar during subjective day and night and decreased with increasing temperature. Paired-pulse stimulation (PPS) and voltage-dependent Ca2+ channel (VDCC) blockers were used to characterize a presynaptic release mechanism. Facilitation was present in 30% and depression in 70% of studied neurons during PPS. Synaptic transmission was reduced by blocking both N- and P/Q-type presynaptic VDCCs, but only the N-type channel blocker significantly relieved SD. Aniracetam inhibited AMPA receptor desensitization but did not alter SD. Thus we concluded that SD is the principal form of short-term plasticity at RHT synapses, which presynaptically and frequency-dependently attenuates light-induced glutamatergic RHT synaptic transmission protecting SCN neurons against excessive excitation.

Sign in / Sign up

Export Citation Format

Share Document