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- W2093174559 abstract "In many neurons, subthreshold somatic depolarization can spread electrotonically into the axon and modulate subsequent spike-evoked transmission. Although release probability is regulated by intracellular Ca(2+), the Ca(2+) dependence of this modulatory mechanism has been debated. Using paired recordings from synaptically connected molecular layer interneurons (MLIs) of the rat cerebellum, we observed Ca(2+)-mediated strengthening of release following brief subthreshold depolarization of the soma. Two-photon microscopy revealed that, at the axon, somatic depolarization evoked Ca(2+) influx through voltage-sensitive Ca(2+) channels and facilitated spike-evoked Ca(2+) entry. Exogenous Ca(2+) buffering diminished these Ca(2+) transients and eliminated the strengthening of release. Axonal Ca(2+) entry elicited by subthreshold somatic depolarization also triggered asynchronous transmission that may deplete vesicle availability and thereby temper release strengthening. In this cerebellar circuit, activity-dependent presynaptic plasticity depends on Ca(2+) elevations resulting from both sub- and suprathreshold electrical activity initiated at the soma." @default.
- W2093174559 created "2016-06-24" @default.
- W2093174559 creator A5012027999 @default.
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- W2093174559 date "2010-12-19" @default.
- W2093174559 modified "2023-10-10" @default.
- W2093174559 title "Ca2+-dependent enhancement of release by subthreshold somatic depolarization" @default.
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- W2093174559 doi "https://doi.org/10.1038/nn.2718" @default.
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