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.

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 Presynaptic Endoplasmic Reticulum Contributes Crucially to Short-term Plasticity in Small Hippocampal Synapses

2018 ◽  
Author(s):  
Nishant Singh ◽  
Thomas Bartol ◽  
Herbert Levine ◽  
Terrence Sejnowski ◽  
Suhita Nadkarni
Keyword(s):  
Endoplasmic Reticulum ◽  
Calcium Influx ◽  
Critical Role ◽  
Presynaptic Terminal ◽  
Calcium Stores ◽  
Pathological State ◽  
Calcium Dynamics ◽  
Short Term ◽  
Short Term Plasticity ◽  
Release Probability

Short-term plasticity (STP) of the presynaptic terminal maintains a brief history of activity experienced by the synapse that may otherwise remain unseen by the postsynaptic neuron. These synaptic changes are primarily regulated by calcium dynamics in the presynaptic terminal. A rapid increase in intracellular calcium is initiated by the opening of voltage-dependent calcium channels in response to depolarization, the main source of calcium required for vesicle fusion. Separately, electron-microscopic studies of hippocampal CA3-CA1 synapses reveal the strong presence of endoplasmic reticulum (ER) in all presynaptic terminals. However, the precise role of the ER in modifying STP at the presynaptic terminal remains unexplored. To investigate the contribution of ER in modulating calcium dynamics in small hippocampal boutons, we performed in silico experiments in a physiologically-realistic canonical synaptic geometry based on reconstructions of CA3-CA1 Schaffer collaterals in the rat hippocampus. The model predicts that presynaptic calcium stores are critical in generating the observed paired-pulse ratio (PPR) of normal CA3-CA1 synapses. In control synapses with intact ER, SERCA pumps act as additional calcium buffers, lowering the intrinsic release probability of vesicle release and increasing PPR. In addition, the presence of ER allows ongoing activity to trigger calcium influx from the presynaptic ER via ryanodine receptors (RyRs) and inositol trisphosphate receptors (IP3Rs). Intracellular stores and their associated machinery also allows a synapse with a low release probability to operate more reliably due to attenuation of calcium fluctuations. Finally, blocking ER activity in the presynaptic terminal mimics the pathological state of a low facilitating synapse characterized in animal models of Alzheimer’s disease, and underscores the critical role played by presynaptic stores in normal function.

Activity-Dependent Increase of the AHP Amplitude in T Sensory Neurons of the Leech

2002 ◽  
Vol 88 (5) ◽  
pp. 2490-2500 ◽  
Author(s):  
Rossana Scuri ◽  
Riccardo Mozzachiodi ◽  
Marcello Brunelli
Keyword(s):  
Sensory Neurons ◽  
Time Window ◽  
Training Session ◽  
Repetitive Stimulation ◽  
Short Term ◽  
Pharmacological Agents ◽  
Stimulus Interval ◽  
Short Term Plasticity ◽  
Intracellular Stimulation ◽  
Activity Dependent

We identified a new form of activity-dependent modulation of the afterhyperpolarization (AHP) in tactile (T) sensory neurons of the leech Hirudo medicinalis. Repetitive intracellular stimulation with 30 trains of depolarizing impulses at 15-s inter-stimulus interval (ISI) led to an increase of the AHP amplitude (∼60% of the control). The enhancement of AHP lasted for ≥15 min. The AHP increase was also elicited when a T neuron was activated by repetitive stimulation of its receptive field. The ISI was a critical parameter for the induction and maintenance of AHP enhancement. ISI duration had to fit within a time window with the upper limit of 20 s to make the training effective to induce an enhancement of the AHP amplitude. After recovery from potentiation, AHP amplitude could be enhanced once again by delivering another training session. The increase of AHP amplitude persisted in high Mg2+ saline, suggesting an intrinsic cellular mechanism for its induction. Previous investigations reported that AHP of leech T neurons was mainly due to the activity of the Na+/K+ ATPase and to a Ca2+-dependent K+ current ( I K/Ca). In addition, it has been demonstrated that serotonin (5HT) reduces AHP amplitude through the inhibition of the Na+/K+ATPase. By blocking the I K/Ca with pharmacological agents, such as cadmium and apamin, we still observed an increase of the AHP amplitude after repetitive stimulation, whereas 5HT application completely inhibited the AHP increment. These data indicate that the Na+/K+ATPase is involved in the induction and maintenance of the AHP increase after repetitive stimulation. Moreover, the AHP increase was affected by the level of serotonin in the CNS. Finally, the increase of the AHP amplitude produced a lasting depression of the synaptic connection between two T neurons, suggesting that this activity-dependent phenomenon might be involved in short-term plasticity associated with learning processes.

scholarly journals Rapid regulation of vesicle priming explains synaptic facilitation despite heterogeneous vesicle:Ca2+ channel distances

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Janus RL Kobbersmed ◽  
Andreas T Grasskamp ◽  
Meida Jusyte ◽  
Mathias A Böhme ◽  
Susanne Ditlevsen ◽  
...  
Keyword(s):  
Super Resolution ◽  
Release Site ◽  
Stochastic Simulations ◽  
Short Term ◽  
Short Term Plasticity ◽  
Release Probability ◽  
Vesicular Release ◽  
Dependent Inhibition ◽  
Super Resolution Microscopy ◽  
Activity Dependent

Chemical synaptic transmission relies on the Ca2+-induced fusion of transmitter-laden vesicles whose coupling distance to Ca2+ channels determines synaptic release probability and short-term plasticity, the facilitation or depression of repetitive responses. Here, using electron- and super-resolution microscopy at the Drosophila neuromuscular junction we quantitatively map vesicle:Ca2+ channel coupling distances. These are very heterogeneous, resulting in a broad spectrum of vesicular release probabilities within synapses. Stochastic simulations of transmitter release from vesicles placed according to this distribution revealed strong constraints on short-term plasticity; particularly facilitation was difficult to achieve. We show that postulated facilitation mechanisms operating via activity-dependent changes of vesicular release probability (e.g. by a facilitation fusion sensor) generate too little facilitation and too much variance. In contrast, Ca2+-dependent mechanisms rapidly increasing the number of releasable vesicles reliably reproduce short-term plasticity and variance of synaptic responses. We propose activity-dependent inhibition of vesicle un-priming or release site activation as novel facilitation mechanisms.

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.

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.

P/Q-type calcium channel ablation in a mice glycinergic synapse mediated by multiple types of Ca2+ channels alters transmitter release and short term plasticity

Neuroscience ◽  
2011 ◽  
Vol 192 ◽  
pp. 219-230 ◽  
Author(s):  
B. Giugovaz-Tropper ◽  
C. González-Inchauspe ◽  
M.N. Di Guilmi ◽  
F.J. Urbano ◽  
I.D. Forsythe ◽  
...  
Keyword(s):  
Calcium Channel ◽  
Transmitter Release ◽  
Short Term ◽  
Short Term Plasticity ◽  
Ca2 Channels

scholarly journals Fast resupply of synaptic vesicles requires Synaptotagmin-3

2021 ◽  
Author(s):  
Dennis J. Weingarten ◽  
Amita Shrestha ◽  
Sarah A. Kissiwaa ◽  
Evan Spruston ◽  
Skyler L. Jackman
Keyword(s):  
Synaptic Transmission ◽  
High Frequency ◽  
Synaptic Vesicles ◽  
Critical Role ◽  
Neuronal Firing ◽  
Probability Models ◽  
Short Term ◽  
Vesicle Docking ◽  
High Affinity ◽  
Readily Releasable Pool

AbstractSustained neuronal activity demands quick resupply of synaptic vesicles in order to maintain reliable synaptic transmission. Such vesicle replenishment is accelerated by sub-micromolar presynaptic Ca2+ signals by an as yet unidentified high-affinity Ca2+ sensor1-4. Here we identify a novel presynaptic role for the high-affinity Ca2+ sensor Synaptotagmin-3 (SYT3)5 in driving vesicle replenishment and short-term synaptic plasticity. Synapses in Syt3 knockout mice exhibit enhanced short-term depression, and recovery is slower and insensitive to presynaptic residual Ca2+. During sustained neuronal firing, SYT3 speeds vesicle replenishment and increases the size of the readily releasable pool of vesicles. SYT3 also mediates a second form of short-term enhancement called facilitation, under conditions of low vesicle release probability. Models of vesicle trafficking suggest that SYT3 could combat synaptic depression by accelerating vesicle docking at active zones. Our results reveal a critical role for presynaptic SYT3 in maintaining reliable high-frequency synaptic transmission in neural circuits.

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