We examined the effect of the Ca
2+ concentration in the endolymph ([Ca]
e) or in the endolymphatic surface cells ([Ca]
i) on the endocochlear potential (EP) by using an endolymphatic or perilymphatic perfusion technique, respectively. (i) A large increase in [Ca]
e up to ∼10
−3 M with a fall in the EP was induced by transient asphyxia (∼2 min) or by the intravenous administration of furosemide (60 mg/kg), and a significant correlation was obtained between the EP and p[Ca]
e (= −log [Ca]
e,
r = 0.998). (ii) Perfusion of the endolymph with 10 mM EGTA for 5 min neither produced any significant change in the EP nor altered the asphyxia-induced change in EP (ΔEP
asp), suggesting that neither [Ca]
e nor the Ca
2+ concentration gradient across the stria vascularis contributed directly to the generation of the EP in the condition of low [Ca]
e. In contrast, endolymphatic perfusion with high Ca
2+ (more than 10 mM) produced a decrease in EP and a significant correlation was obtained between the EP and the Ca
2+ concentration of perfusion solution (
r = 0.982), suggesting that Ca
2+ permeability may exist across the stria vascularis. (iii) The administration of a Ca
2+ chelator, EGTA-acetoxymethyl ester (AM, 0.3 mM), to the endolymph, which produced a gradual increase in EP, suppressed significantly, by 60–80%, ΔEP
asp or furosemide-induced changes in EP. In contrast, perilymphatic administration of 0.5 mM EGTA-AM caused no significant suppression of the ΔEP
asp. These findings suggest that [Ca]
i plays an important role in generating/maintaining a large positive EP.
抄録全体を表示