Calcium from internal stores triggers GABA release from retinal amacrine cells

Warrier, Ajithkumar, Salvador Borges, David Dalcino, Cameron Walters, and Martin Wilson. Calcium from internal stores triggers GABA release from retinal amacrine cells. J Neurophysiol 94: 4196-4208, 2005; doi: 10.1152/jn. 00604.2005. 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 (IP(3)Rs) 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 IP(3)Rs, 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.