Short-Term Synaptic Plasticity

Abstract

Synaptic transmission is a dynamic process. Postsynaptic responses wax and wane as presynaptic activity evolves. This prominent characteristic of chemical synaptic transmission is a crucial determinant of the response properties of synapses and, in turn, of the stimulus properties selected by neural networks and of the patterns of activity generated by those networks. This review focuses on synaptic changes that result from prior activity in the synapse under study, and is restricted to short-term effects that last for at most a few minutes. Forms of synaptic enhancement, such as facilitation, augmentation, and post-tetanic potentiation, are usually attributed to effects of a residual elevation in presynaptic [Ca(2+)]i, acting on one or more molecular targets that appear to be distinct from the secretory trigger responsible for fast exocytosis and phasic release of transmitter to single action potentials. We discuss the evidence for this hypothesis, and the origins of the different kinetic phases of synaptic enhancement, as well as the interpretation of statistical changes in transmitter release and roles played by other factors such as alterations in presynaptic Ca(2+) influx or postsynaptic levels of [Ca(2+)]i. Synaptic depression dominates enhancement at many synapses. Depression is usually attributed to depletion of some pool of readily releasable vesicles, and various forms of the depletion model are discussed. Depression can also arise from feedback activation of presynaptic receptors and from postsynaptic processes such as receptor desensitization. In addition, glial-neuronal interactions can contribute to short-term synaptic plasticity. Finally, we summarize the recent literature on putative molecular players in synaptic plasticity and the effects of genetic manipulations and other modulatory influences.

Memristor with Ag‐Cluster‐Doped TiO2 Films as Artificial Synapse for Neuroinspired Computing

“…[3] Biologically, the synaptic weight is analog plastic, which correspond to the connection strength of neurons. STDP is one most important Hebbian learning rule for learning and memory, [39,40] meaning that the synaptic weight can be controlled by the relative timing of pre-and postsynaptic spikes.…”

“…[12] PPF is another kind of main parameter, which can manifest the temporal summation on inputs for biological synapses. [40] Figure 5c dependence of synaptic weight and pulse intervals. The pulse with amplitude of −0.5 and 0.4 V was applied on the Ag/TiO 2 :Ag/Pt device, as shown in Figure 5c,d, respectively.…”

Ca2+-induced Recruitment of the Secretory Vesicle Protein DOC2B to the Target Membrane

“…Estimated concentrations of intracellular Ca 2ϩ in neurons range from 10 -100 M during Ca 2ϩ channel opening to ϳ1 M during delayed phases after Ca 2ϩ influx and ϳ100 nm under resting conditions (2,27). The peak levels are only reached transiently (for milliseconds) in close proximity to activated Ca 2ϩ channels.…”

Distinct target cell-dependent forms of short-term plasticity of the central visceral afferent synapses of the rat

“…The classification of type I and type II DMX neurons as shown in Figure 1C was determined according to the PPR with an inter-stimulus interval (ISI) of 100 ms at 2 mM [Ca 2+ ] o . As has been commonly described [29,30], the PPR value changed as we changed ISI from 20 ms to 10 s (Figure 3). However, despite such ISI-dependent modulation of PPR, the ISI-PPR plot (Figure 3B) indicates that the PPR-dependent classification between NTS, type I and type II DMX neurons was relatively resistant to the changes in ISI.…”

“…While the properties of the type II DMX synapses described in this study favor short-term depression primarily due to large P r , more frequent multi-vesicular release, and a smaller pool of docked vesicles [40,29,30], the properties of TS-type I DMX neuron synapses with much less short-term depression or rather facilitation in response to both submaximal and minimal stimulation are likely to result from small P r and a sufficient number of vesicles that are ready for exocytosis even after a short period of time. It will therefore be necessary for future studies to identify the molecular determinants of such distinct short-term plasticity in these DMX synapses [30].…”