Ca2+-dependent enhancement of release by subthreshold somatic depolarization

Jason M. Christie, Delia N. Chiu, Craig E. Jahr

Research output: Contribution to journalArticle

74 Scopus citations

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 Ca2+ 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 Ca2+ influx through voltage-sensitive Ca2+ channels and facilitated spike-evoked Ca2+ entry. Exogenous Ca2+ buffering diminished these Ca2+ transients and eliminated the strengthening of release. Axonal Ca2+ 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 Ca2+ elevations resulting from both sub- and suprathreshold electrical activity initiated at the soma.

Original languageEnglish (US)
Pages (from-to)62-69
Number of pages8
JournalNature Neuroscience
Volume14
Issue number1
DOIs
StatePublished - Jan 1 2011

ASJC Scopus subject areas

  • Neuroscience(all)

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