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Department of Physiology, School of Medicine, Akita University, Japan.

1. Ryanodine-sensitive intracellular Ca2+ release activated by Ca2+ entry was studied with fura-2 fluorescence and intracellular voltage recording techniques in rabbit otic ganglion cells. 2. The removal of extracellular Ca2+ reduced sustained, transient or oscillatory rises in intracellular Ca2+ ([Ca2+]i) induced at high extracellular K+ and abolished the [Ca2+]i oscillation in cultured neurones. 3. Ryanodine (10 microM) transiently increased [Ca2+]i and reduced the amplitude and rate of rise of the high-K(+)-induced rise in [Ca2+]i, while caffeine (5 mM) produced a few transient rises in [Ca2+]i in most cultured cells and [Ca2+]i oscillation only in one cell. 4. The two components of the slow after-hyperpolarization (AHP) of an action potential in neurones of freshly isolated ganglia were dependent on extracellular Ca2+ and abolished by Ca2+ channel blockers, Cd2+ or Co2+. 5. The late component of AHP (LAHP), but not the initial component, in 'fresh' neurones increased in area with an increase in the preceding interval, was abolished by ryanodine (10 microM) and intracellularly injected EGTA, and mimicked by intracellular injection of Ca2+. 6. A ryanodine-sensitive Ca(2+)-induced Ca2+ release thus exists, operates in response to an action potential-induced Ca2+ entry and underlies LAHP in rabbit otic ganglion cells.

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