The role of potassium and sodium in cochlear transduction: A study with amiloride and tetraethylammonium

Abstract

The effects of amiloride and tetraethylammonium (TEA) on cochlear microphonics (CM), action potentials (AP), and endocochlear potential (EP) were studied in guinea pigs. It has been reported that amiloride selectively reduces sodium permeability in a variety of ion transporting epithelia. Perilymphatic perfusion (10−3 M) or intravenous administration (20 mg/kg) of amiloride suppressed AP, but did not significantly alter CM or EP. Application of amiloride to the endolymph by iontophoretic or perfusion techniques also produced no greater changes of CM and EP than were observed during control procedures. TEA has been shown to suppress the potassium permeability increase in excitable cell membranes. Perilymphatic perfusion of TEA (10‐2 M) did not suppress CM or EP, but AP was reduced. Iontophoretic application of TEA to the endolymph markedly suppressed CM, while EP increased in value. The effects of TEA applied to the endolymph were similar to those effects previously reported to occur during noise exposure (J. Acoust. Soc. Am. Suppl. 1 64, S132(A) (1978)]. This result adds support to the hypothesis that noise induced CM suppression is a consequence of a potassium permeability decrease of the endolymph/perilymph barrier. The contribution of sodium ion movements to cochlear transduction appears less certain in the light of the insensitivity of CM and EP to amiloride.