Short-term forms of presynaptic plasticity

Abstract

Synapses exhibit several forms of short-term plasticity that play a multitude of computational roles. Short-term depression suppresses neurotransmitter release for hundreds of milliseconds to tens of seconds; facilitation and post-tetanic potentiation lead to synaptic enhancement lasting hundreds of milliseconds to minutes. Recent advances have provided insight into the mechanisms underlying these forms of plasticity. Vesicle depletion and inactivation of release sites and calcium channels contribute to synaptic depression. Mechanisms of short-term enhancement include calcium channel facilitation, local depletion of calcium buffers, increases in the probability of release downstream of calcium influx, altered vesicle pool properties, and increases in quantal size. Moreover, there is a growing appreciation of the heterogeneity of vesicles and release sites and how they can contribute to use-dependent plasticity.

Calcium sensor regulation of the Ca V 2.1 Ca 2+ channel contributes to long-term potentiation and spatial learning

“…1B). Potentiation immediately following the tetanus was similar for WT and IM-AA (WT, 265 ± 36%; IM-AA, 295 ± 33%), which is expected because posttetanic potentiation does not involve calcium channel regulation (3,13). On the other hand, excitatory postsynaptic current (EPSC) amplitude was sustained in WT but decreased rapidly in IM-AA to only 122 ± 18% of the pretetanus value by 60 min after the end of the tetanic stimulus (Fig.…”

“…Short-term and long-term modifications in synaptic strength are regulated by the frequency and pattern of presynaptic spiking (2)(3)(4)(5). Regulation of voltage-gated Ca 2+ channel type 2.1 (Ca V 2.1) by calmodulin (CaM) and related Ca 2+ sensor (CaS) proteins causes Ca 2+ -dependent facilitation and inactivation of P/Qtype Ca 2+ currents (6)(7)(8)(9)(10)(11)(12) that results in short-term facilitation and rapid depression of synaptic transmission (9,(12)(13)(14).…”

Site-Specific Synapsin I Phosphorylation Participates in the Expression of Post-Tetanic Potentiation and Its Enhancement by BDNF

“…PTP is a form a short-term synaptic plasticity involving the activity-dependent mobilization of the SV recycling pool in which the potential role of SynI has been controversial (Zucker and Regehr, 2002;Fioravante and Regehr, 2011). To analyze the molecular mechanisms of PTP expression, we studied the potential role of SynI and its phosphorylation as a presynaptic target of HFS in excitatory autapses from the hippocampus of WT and KO mice (Fig.…”

“…Post-tetanic potentiation (PTP) is a transient enhancement of synaptic strength in response to high-frequency stimulation (HFS) which is associated with an increased number of neurotransmitter quanta released in response to the action potential (Zucker and Regehr, 2002). Distinct quantal mechanisms contribute to PTP in various synapses and several presynaptic candidates have been implicated in the expression of PTP, including synapsins, Munc13, Ca 2ϩ -activated kinases, or Ca 2ϩ -binding proteins (Fioravante and Regehr, 2011).…”

Error correction and fast detectors implemented by ultrafast neuronal plasticity

“…Shortterm synaptic plasticity reflects an increase (facilitation) and decrease (depression) in the probability of neurotransmitter release [3,4]. It affects the speed of synaptic signal transmission and can last from hundreds of milliseconds to seconds [3,5]. This phenomenon varies enormously depending on the neuronal and synaptic features as well as on the neuron's recent history of activity [6][7][8].…”