2-chloro-5-hydroxyphenylglycine and 2-aminoethoxydiphenyl-borate

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.

Topics: Amacrine Cells; Animals; Boron Compounds; Caffeine; Calcium; Calcium Channels; Calcium-Binding Proteins; Central Nervous System Stimulants; Chick Embryo; Diagnostic Imaging; Dose-Response Relationship, Drug; Drug Interactions; Electric Stimulation; Endoplasmic Reticulum; Evoked Potentials; Excitatory Amino Acid Agonists; gamma-Aminobutyric Acid; Glycine; Heparin; Immunohistochemistry; Inositol 1,4,5-Trisphosphate Receptors; Membrane Potentials; Microscopy, Confocal; Organic Chemicals; Patch-Clamp Techniques; Phenylacetates; Receptors, Cytoplasmic and Nuclear; Retina; Ryanodine; Ryanodine Receptor Calcium Release Channel; Time Factors