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 Ca 2+ that promotes transmitter release is generally thought to enter presynaptic terminals through voltage-gated Ca 2+ channels. Using electrophysiology and Ca 2+ imaging, we show that, in amacrine cell dendrites, at least some of the Ca 2+ that triggers transmitter release comes from endoplasmic reticulum Ca 2+ stores. We show that both inositol 1,4,5-trisphosphate receptors (IP 3 Rs) and ryanodine receptors (RyRs) are present in these dendrites and both participate in the elevation of cytoplasmic [Ca 2+ ] during the brief depolarization of a dendrite. Only the Ca 2+ released through IP 3 Rs, however, seems to promote the release of transmitter. Antagonists for the IP 3 R reduced transmitter release, whereas RyR blockers had no effect. Application of an agonist for metabotropic glutamate receptor, known to liberate Ca 2+ from internal stores, enhanced both spontaneous and evoked transmitter release. Address for reprint requests and other correspondence: M. Wilson, Section of Neurobiology, Physiology and Behavior, Div. of Biological Sciences, UC Davis, Davis, CA 95616 (E-mail: mcwilson{at}ucdavis.edu )