抄録
We examined the effect of the Ca2+ concentration in the endolymph ([Ca]e) or in the endolymphatic surface cells on the endocochlear potential (EP) by using Ca2+-selective and conventional microelectrodes. 1) The abrupt increase in [Ca]e up to ∼10−3 M with a fall in the EP was induced by transient asphyxia (∼1.5 min) or intravenous administration of furosemide (60 mg/kg), and significant correlation was obtained between the EP and p[Ca] e (= –log [Ca] e). 2) The perfusion of endolymph with 10 mM EGTA-containing solution for 5 min neither produced any significant change in the EP nor altered the asphyxia-induced change in EP, suggesting that Ca2+ concentration across the stria vascularis did not contributed directly to the generation of EP. 3) The administration of 300 µM EGTA-tetraacetoxymethyl ester (EGTA-AM) with 10 mM EGTA-containing solution to the endolymph produced a gradual increase in EP and suppressed the asphyxia or furosemide-induced decrease in EP, although perilymphatic administration of 1 mM EGTA-AM caused no significant suppression of the asphyxia-induced change in EP. 4) The application of 30 μM nifedipine to perilymph also suppressed the fall in EP induced by transient asphyxia. These findings indicated that Ca2+ homeostasis in the stria vascularis cells plays an important role in generating/maintaining a large positive EP. [Jpn J Physiol 55 Suppl:S157 (2005)]
