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The effect of thapsigargin and ryanodine on cochlear microphonics (CM) and the endocochlear DC potential (EP) in the guinea pig was investigated by the perilymphatic perfusion method. These chemicals were considered to be pharmacological tools to reduce the amount of Ca2+ stored within the endoplasmic reticulum (ER), although the sites of their action were different; thapsigargin inhibits Ca2+ uptake of the ER, while ryanodine locks Ca2+ channels of the ER in an open state. Both CM and EP were measured with a glass microelectrode inserted into scala media. The amplitude of CM started to decrease soon after the beginning of thapsigargin perfusion and fell to 35% of the initial value in 30 minutes. Ryanodine, like thapsigargin, reduced the CM amplitude depending on the concentration between 1 x 10(-6) approximately 3 x 10(-5)M. These results suggest that Ca2+ ions which regulate the ciliar movements of outer hair cells are due not only to entry from extracellular fluid but to their release from the intracellular storage sites, probably through the mechanisms of Ca(2+)-induced Ca2+ release.

EFFECTS OF THAPSIGARGIN AND RYANODINE ON COCHLEAR ELECTRICAL POTENTIALS IN GUINEA PIGS EXAMINED BY THE PERILYMPHATIC PERFUSION METHOD