Effect of CO₂/HCO₃⁻ on endocochlear potential in guinea pigs

Abstract

Pendred syndrome, characterized by deafness and goiter, is caused by the mutation of the PDS gene SLC26A4, which codes for the pendrin. This protein is an anion exchenger, which can transport Cl⁻ and HCO₃⁻, has been found in the endolymphatic surface cells. Recent study demonstrated that positive endocochlear potential (EP) was disappeared in Slc26a4^−/− mice. In the present study, therefore, we examined the effect of CO₂/HCO₃⁻ on EP by using perilymphatic or endolymphatic perfusion technique in guinea pigs. The gradual decrease in EP from 70 to 25 mV was induced by a perilymphatic perfusion of CO₂/HCO₃⁻-free (Hepes buffer) solution. In this condition a transient asphyxia for ∼2 min produced further decrease in EP to -10 mV, whereas it produced the decrease in EP from 80 to 20 mV with the perilymphatic perfusion of 5% CO₂/25 mM HCO₃⁻ solution. The perfusion of perilymph or endolymph with 30 μM nifedipine suppressed the both Hepes buffer-induced decrease (HBID) or transient asphyxia-induced decrease (TAID) in EP. By contrast, perilymphatic administration of La³⁺ produced a decrease in EP and no significant suppression of HBID or TAID in EP. Perilymphatic administration of 1 mM EGTA-tetraacetoxymethyl ester (EGTA-AM) produced no significant suppression of HBID or TAID in EP. These findings suggest that effect of CO₂/HCO₃⁻ on EP is mediated by Ca²⁺ homeostasis in the cell of stria vascularis, especially by the nifedipine-sensitive Ca²⁺ channel. [Jpn J Physiol 55 Suppl:S158 (2005)]