A study on the mechanism of intracellular Ca^<2+> release in neurones and its physiological functions.

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The mechanism of intracellular Ca^<2+> release and its physiological functions were studied in cultured bullfrog sympathetic and rabbit otic ganglion cells, using fura-2 or indo-1 fluorescence redording techniques with a photomultiplier or confocal laser-scanning microscope and shole cell patch clamp techniques. Ryanodine-sensitive Ca^<2+> -induced Ca^<2+> release (CICR) in bullfrog sympathetic neurones were voltage-dependently activated throughout the cytoplasm by Ca^<2+> influx produced by a depolarizing voltage pulse (> 100 ms), but only in the submembrane regions by Ca^<2+> influx caused by action potentials (> 10 Hz, 100 pulses). Under the effects of intracellular cyclic ADP-ribose, tetanic action potentials activated propagating CICR.iIn cultured rabbit otic ganglion cells, when the extracellular Ca^<2+> was reduced to a level < 0.1 mM, a small Ca^<2+> entry produced by a high K^+ -induced depolarization caused a propagating Ca^<2+> release from mitochondria which was blocked by cyclosprin A.These two mechanisms may operate in ceurones in situ depending on the extracellular Ca^<2+> levels that would be altered by activities of neighboring neurones.