Author

Delia N. Chiu

Date

9-2014

Document Type

Dissertation

Degree Name

Ph.D.

Institution

Oregon Health & Science University

Abstract

In many neurons, subthreshold somatic depolarization can spread lectrotonically 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. Twophoton microscopy revealed that, at the axon, somatic depolarization evoked Ca 2+ influx through voltage-sensitive Ca 2+ channels (VSCCs) and facilitated spike-evoked Ca2+ entry. Exogenous Ca 2+ buffering diminished these Ca2+ transients and eliminated the strengthening of release. Axonal Ca 2+ entry elicited by subthreshold somatic epolarization 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.

Identifier

doi:10.6083/M4HT2N28

Division

Neuroscience Graduate Program

School

School of Medicine

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