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Calcium From Internal Stores Triggers GABA Release From Retinal Amacrine Cells

Section of Neurobiology, Physiology and Behavior, Division of Biological Sciences, University of California, Davis, California

Submitted 10 June 2005; accepted in final form 17 August 2005

The Ca²⁺ that promotes transmitter release is generally thought to enter presynaptic terminals through voltage-gated Ca²⁺channels. Using electrophysiology and Ca²⁺ imaging, we show that, in amacrine cell dendrites, at least some of the Ca²⁺ that triggers transmitter release comes from endoplasmic reticulum Ca²⁺ stores. We show that both inositol 1,4,5-trisphosphate receptors (IP₃Rs) and ryanodine receptors (RyRs) are present in these dendrites and both participate in the elevation of cytoplasmic [Ca²⁺] during the brief depolarization of a dendrite. Only the Ca²⁺ released through IP₃Rs, however, seems to promote the release of transmitter. Antagonists for the IP₃R reduced transmitter release, whereas RyR blockers had no effect. Application of an agonist for metabotropic glutamate receptor, known to liberate Ca²⁺ from internal stores, enhanced both spontaneous and evoked transmitter release.

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				S. Borges, S. Lindstrom, C. Walters, A. Warrier, and M. Wilson Discrete influx events refill depleted Ca2+ stores in a chick retinal neuron J. Physiol., January 15, 2008; 586(2): 605 - 626. [Abstract] [Full Text] [PDF]