Structural Contributions to Short-Term Synaptic Plasticity

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.

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Skipped-Stimulus Approach Reveals That Short-Term Plasticity Dominates Synaptic Strength during Ongoing Activity

Journal of Neuroscience ◽

10.1523/jneurosci.4299-14.2015 ◽

2015 ◽

Vol 35 (21) ◽

pp. 8297-8307 ◽

Cited By ~ 8

Author(s):

H. Yang ◽

M. A. Xu-Friedman

Keyword(s):

Synaptic Strength ◽

Short Term ◽

Ongoing Activity ◽

Short Term Plasticity

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Synaptotagmin 7 switches short-term synaptic plasticity from depression to facilitation by suppressing synaptic transmission

Scientific Reports ◽

10.1038/s41598-021-83397-5 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Takaaki Fujii ◽

Akira Sakurai ◽

J. Troy Littleton ◽

Motojiro Yoshihara

Keyword(s):

Synaptic Plasticity ◽

Synaptic Transmission ◽

Synaptic Vesicle ◽

Neuromuscular Junctions ◽

Binding Protein ◽

Repetitive Stimulation ◽

Evoked Response ◽

Short Term ◽

Short Term Plasticity ◽

Null Mutants

AbstractShort-term synaptic plasticity is a fast and robust modification in neuronal presynaptic output that can enhance release strength to drive facilitation or diminish it to promote depression. The mechanisms that determine whether neurons display short-term facilitation or depression are still unclear. Here we show that the Ca2+-binding protein Synaptotagmin 7 (Syt7) determines the sign of short-term synaptic plasticity by controlling the initial probability of synaptic vesicle (SV) fusion. Electrophysiological analysis of Syt7 null mutants at Drosophila embryonic neuromuscular junctions demonstrate loss of the protein converts the normally observed synaptic facilitation response during repetitive stimulation into synaptic depression. In contrast, overexpression of Syt7 dramatically enhanced the magnitude of short-term facilitation. These changes in short-term plasticity were mirrored by corresponding alterations in the initial evoked response, with SV release probability enhanced in Syt7 mutants and suppressed following Syt7 overexpression. Indeed, Syt7 mutants were able to display facilitation in lower [Ca2+] where release was reduced. These data suggest Syt7 does not act by directly sensing residual Ca2+ and argues for the existence of a distinct Ca2+ sensor beyond Syt7 that mediates facilitation. Instead, Syt7 normally suppresses synaptic transmission to maintain an output range where facilitation is available to the neuron.

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Frequency-Dependent Modulation of Short-Term Plasticity of GABAergic Synaptic Transmission

International Journal of Physiology and Pathophysiology ◽

10.1615/intjphyspathophys.v9.i2.30 ◽

2018 ◽

Vol 9 (2) ◽

pp. 119-126

Author(s):

Oksana P. Kolesnyk ◽

Svetlana A. Fedulova ◽

Mycola S. Veselovsky

Keyword(s):

Synaptic Transmission ◽

Short Term ◽

Frequency Dependent ◽

Short Term Plasticity ◽

Gabaergic Synaptic Transmission

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Synapsin Regulates Basal Synaptic Strength, Synaptic Depression, and Serotonin-Induced Facilitation of Sensorimotor Synapses in Aplysia

Journal of Neurophysiology ◽

10.1152/jn.00604.2007 ◽

2007 ◽

Vol 98 (6) ◽

pp. 3568-3580 ◽

Cited By ~ 14

Author(s):

Diasinou Fioravante ◽

Rong-Yu Liu ◽

Anne K. Netek ◽

Leonard J. Cleary ◽

John H. Byrne

Keyword(s):

Synaptic Plasticity ◽

Synaptic Vesicle ◽

Transmitter Release ◽

Computational Analysis ◽

Spontaneous Recovery ◽

Synaptic Strength ◽

Short Term ◽

Homosynaptic Depression ◽

Heterosynaptic Plasticity

Synapsin is a synaptic vesicle-associated protein implicated in the regulation of vesicle trafficking and transmitter release, but its role in heterosynaptic plasticity remains elusive. Moreover, contradictory results have obscured the contribution of synapsin to homosynaptic plasticity. We previously reported that the neuromodulator serotonin (5-HT) led to the phosphorylation and redistribution of Aplysia synapsin, suggesting that synapsin may be a good candidate for the regulation of vesicle mobilization underlying the short-term synaptic plasticity induced by 5-HT. This study examined the role of synapsin in homosynaptic and heterosynaptic plasticity. Overexpression of synapsin reduced basal transmission and enhanced homosynaptic depression. Although synapsin did not affect spontaneous recovery from depression, it potentiated 5-HT–induced dedepression. Computational analysis showed that the effects of synapsin on plasticity could be adequately simulated by altering the rate of Ca2+-dependent vesicle mobilization, supporting the involvement of synapsin not only in homosynaptic but also in heterosynaptic forms of plasticity by regulating vesicle mobilization.

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A General Model of Synaptic Transmission and Short-Term Plasticity

Neuron ◽

10.1016/j.neuron.2009.03.025 ◽

2009 ◽

Vol 62 (4) ◽

pp. 539-554 ◽

Cited By ~ 105

Author(s):

Bin Pan ◽

Robert S. Zucker

Keyword(s):

Synaptic Transmission ◽

General Model ◽

Short Term ◽

Short Term Plasticity

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Sevoflurane Blocks Cholinergic Synaptic Transmission Postsynaptically but Does Not Affect Short-term Potentiation

Anesthesiology ◽

10.1097/00000542-200505000-00010 ◽

2005 ◽

Vol 102 (5) ◽

pp. 920-928 ◽

Cited By ~ 17

Author(s):

Hiroaki Naruo ◽

Shin Onizuka ◽

David Prince ◽

Mayumi Takasaki ◽

Naweed I. Syed

Keyword(s):

Synaptic Plasticity ◽

Synaptic Transmission ◽

Fluorescent Imaging ◽

Posttetanic Potentiation ◽

Dependent Manner ◽

General Anesthetics ◽

Short Term ◽

Concentration Dependent Manner ◽

Cholinergic Synaptic Transmission ◽

Term Potentiation

Background As compared with their effects on both inhibitory and excitatory synapses, little is known about the mechanisms by which general anesthetics affect synaptic plasticity that forms the basis for learning and memory at the cellular level. To test whether clinically relevant concentrations of sevoflurane affect short-term potentiation involving cholinergic synaptic transmission, the soma-soma synapses between identified, postsynaptic neurons were used. Methods Uniquely identifiable neurons visceral dorsal 4 (presynaptic) and left pedal dorsal 1 (postsynaptic) of the mollusk Lymnaea stagnalis were isolated from the intact ganglion and paired overnight in a soma-soma configuration. Simultaneous intracellular recordings coupled with fluorescent imaging of the FM1-43 dye were made in either the absence or the presence of sevoflurane. Results Cholinergic synapses, similar to those observed in vivo, developed between the neurons, and the synaptic transmission exhibited classic short-term, posttetanic potentiation. Action potential-induced (visceral dorsal 4), 1:1 excitatory postsynaptic potentials were reversibly and significantly suppressed by sevoflurane in a concentration-dependent manner. Fluorescent imaging with the dye FM1-43 revealed that sevoflurane did not affect presynaptic exocytosis or endocytosis; instead, postsynaptic nicotinic acetylcholine receptors were blocked in a concentration-dependent manner. To test the hypothesis that sevoflurane affects short-term potentiation, a posttetanic potentiation paradigm was used, and synaptic transmission was examined in either the presence or the absence of sevoflurane. Although 1.5% sevoflurane significantly reduced synaptic transmission between the paired cells, it did not affect the formation or retention of posttetanic potentiation at this synapse. Conclusions This study demonstrates that sevoflurane blocks cholinergic synaptic transmission postsynaptically but does not affect short-term synaptic plasticity at the visceral dorsal 4-left pedal dorsal 1 synapse.

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A model of order-selectivity based on dynamic changes in the balance of excitation and inhibition produced by short-term synaptic plasticity

Journal of Neurophysiology ◽

10.1152/jn.00568.2014 ◽

2015 ◽

Vol 113 (2) ◽

pp. 509-523 ◽

Cited By ~ 14

Author(s):

Vishwa Goudar ◽

Dean V. Buonomano

Keyword(s):

Synaptic Plasticity ◽

Computational Models ◽

Experimental Studies ◽

Inhibitory Synapses ◽

Speech Discrimination ◽

Short Term ◽

Dynamic Changes ◽

Short Term Plasticity ◽

Underlying Mechanisms ◽

Parametric Analyses

Determining the order of sensory events separated by a few hundred milliseconds is critical to many forms of sensory processing, including vocalization and speech discrimination. Although many experimental studies have recorded from auditory order-sensitive and order-selective neurons, the underlying mechanisms are poorly understood. Here we demonstrate that universal properties of cortical synapses—short-term synaptic plasticity of excitatory and inhibitory synapses—are well suited for the generation of order-selective neural responses. Using computational models of canonical disynaptic circuits, we show that the dynamic changes in the balance of excitation and inhibition imposed by short-term plasticity lead to the generation of order-selective responses. Parametric analyses predict that among the forms of short-term plasticity expressed at excitatory-to-excitatory, excitatory-to-inhibitory, and inhibitory-to-excitatory synapses, the single most important contributor to order-selectivity is the paired-pulse depression of inhibitory postsynaptic potentials (IPSPs). A topographic model of the auditory cortex that incorporates short-term plasticity accounts for both context-dependent suppression and enhancement in response to paired tones. Together these results provide a framework to account for an important computational problem based on ubiquitous synaptic properties that did not yet have a clearly established computational function. Additionally, these studies suggest that disynaptic circuits represent a fundamental computational unit that is capable of processing both spatial and temporal information.

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Translational control of synaptic plasticity

Biochemical Society Transactions ◽

10.1042/bst0381527 ◽

2010 ◽

Vol 38 (6) ◽

pp. 1527-1530 ◽

Cited By ~ 14

Author(s):

Joel D. Richter

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Synaptic Plasticity ◽

Synaptic Transmission ◽

Learning And Memory ◽

Translational Control ◽

Synaptic Strength ◽

Memory Formation ◽

The Central Nervous System ◽

Flow Of Information

Synapses, points of contact between axons and dendrites, are conduits for the flow of information in the circuitry of the central nervous system. The strength of synaptic transmission reflects the interconnectedness of the axons and dendrites at synapses; synaptic strength in turn is modified by the frequency with which the synapses are stimulated. This modulation of synaptic strength, or synaptic plasticity, probably forms the cellular basis for learning and memory. RNA metabolism, particularly translational control at or near the synapse, is one process that controls long-lasting synaptic plasticity and, by extension, memory formation and consolidation. In the present paper, I review some salient features of translational control of synaptic plasticity.

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