CA2-INDUCED CA2+ RELEASE AND ITS ACTIVATION IN RESPONSE TO A SINGLE ACTION-POTENTIAL IN RABBIT OTIC GANGLION-CELLS()

1. Ryanodine-sensitive intracellular Ca2+ release activated by Ca2+ en try was studied with fura-2 fluorescence and intracellular voltage rec ording techniques in rabbit otic ganglion cells. 2. The removal of ext racellular Ca2+ reduced sustained, transient or oscillatory rises in i ntracellular Ca2+ ([Ca2+](1)) induced at high extracellular K+ and abo lished the [Ca,2+](i) oscillation in cultured neurones. 3. Ryanodine ( 10 mu M) transiently increased [Ca2+](1) 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+](1) in most cultured c ells and [Ca2+](i) oscillation only in one cell. 4. The two components of the slow after-hyperpolarization (AHP) of an action potential in n eurones of freshly isolated ganglia were dependent on extracellular Ca 2+ and abolished by Ca2+ channel blockers, Cd2+ or Co2+. 5. The late c omponent of AHP (LAHP), but not the initial component, in 'fresh' neur ones increased in area with an increase in the preceding interval, was abolished by ryanodine (10 mu M) and intracellularly injected EGTA, a nd mimicked by intracellular injection of Ca2+. 6. A ryanodine-sensiti ve Ca2+-induced Ca2+ release thus exists, operates in response to an a ction potential-induced Ca2+ entry and underlies LAHP in rabbit otic g anglion cells.