Potassium-Induced Release of Endogenous Amino Acids in the Guinea Pig Cochlea

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Abstract
Guinea pig cochleae were perfused with high-K solutions to depolarize hair cells artificially and induce the release of afferent neurotransmitter. Sequential injections of artificial perilymph containing 5 m M KCl, then 50 m M KCl and finally 5 m M KCl were made into the scala tympani. This injection sequence was conducted under either normal divalent-cation conditions (2.0 m M Ca Cl2, 1.0 m M Mg Cl2). The levels of 21 endogenous primary amines in effluent collected from the scala vestibuli were determined by gradient-elution, reverse-phase HPLC [high performance liquid chromatography] using o-phthaldialdehyde-thiol adducts with fluorescence detection. Analysis indicated effluent concentrations of glutamate, taurine and a coeluting taurine-.gamma.-aminobutyrate (GABA) fraction (but not GABA alone) increased significantly after exposure to 50 m M KCl and returned to baseline levels after reintroduction of 5 m M KCl under normal divalent-cation conditions. Correspondent changes in the release of these constituents were significantly attenuated under Ca-deficient conditions. This was not the case for K-induced changes in the release of arginine, aspartate and isoleucine. The receptoneuronal transmitter is glutamate, a Ca-dependent mechanism involving taurine is suggested.