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Fast changes in the functional status of release sites during short‐term plasticity: involvement of a frequency‐dependent bypass of Rac at Aplysia synapses
Author(s) -
Humeau Yann,
Doussau Frédéric,
Popoff Michel R.,
Benfenati Fabio,
Poulain Bernard
Publication year - 2007
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2007.139899
Subject(s) - postsynaptic potential , long term potentiation , neuroscience , neurotransmission , aplysia , synaptic plasticity , inhibitory postsynaptic potential , extracellular , biology , biophysics , chemistry , microbiology and biotechnology , biochemistry , receptor
Synaptic transmission can be described as a stochastic quantal process defined by three main parameters: N , the number of functional release sites; P , the release probability; and Q , the quantum of response. Many changes in synaptic strength that are observed during expression of short term plasticity rely on modifications in P . Regulation of N has been also suggested. We have investigated at identified cholinergic inhibitory Aplysia synapses the cellular mechanism of post‐tetanic potentiation (PTP) expressed under control conditions or after N has been depressed by applying lethal toxin (LT) from Clostridium sordellii or tetanus toxin (TeNT). The analysis of the Ca 2+ dependency, paired‐pulse ratio and variance to mean amplitude relationship of the postsynaptic responses elicited at distinct extracellular [Ca 2+ ]/[Mg 2+ ] elicited during control post‐tetanic potentiation (PTP cont ) indicated that PTP cont is mainly driven by an increase in release probability, P . The PTP expressed at TeNT‐treated synapses (PTP TeNT ) was found to be similar to PTP cont , but scaled to the extent of reduction in N produced by TeNT. Despite LT inducing a decrease in N as TeNT does, the PTP expressed at LT‐treated synapses (PTP LT ) was characterized by exceptionally large amplitude and bi‐exponential time course, as compared to PTP cont or the PTP TeNT . Analysis of the Ca 2+ dependency of PTP LT , paired‐pulse ratio and fluctuations in amplitude of the postsynaptic responses elicited during PTP LT or the variance to mean amplitude relationship of time‐locked postsynaptic responses in a series of subsequent PTP LT indicated that an N‐ driven change is involved in the early phase (1 s time scale) of PTP LT , while at a later stage PTP LT is composed of both N and P increases. Our results suggest that fast switching on of the functional status of the release sites occurs also during the early events of PTP cont . The early N ‐driven phase of PTP LT is likely to be a functional recovery of the release sites silenced by Rac inactivation. This effect did not appear to result from reversion of LT inhibitory action but from bypassing the step regulated by Rac. Altogether the data suggest that Rac and the intracellular pathway which allows the bypassing of Rac are key players in new forms of short‐term plasticity that rely on fast, activity‐dependent changes in the functional status of the release sites.