Potassium‐induced release of glutamate and taurine into perilymph is calcium‐dependent

Perfusion of the choclea with artificial perilymph containing high concentrations of potassium chloride selectively induces the release of several different endogenous amino acids [Neurosci. Abstr. 16.1 (1983)]. This study examines whether such augmentations reflect the liberation of neurotransmitter(s) from depolarized hair cells by comparing potassium‐induced changes in amino acid levels evoked under normal divalent ion conditions $(2.0 mM Ca+2−1.0 mM Mg+2)$ to the effects of potassium elicited under conditions known to antagonize evoked transmitter release $(0.1 mM Ca+2−20.0 mM Mg+2)$⁠. For each condition, high performance liquid chromatographic analyses were conducted on artificial perilymph samples collected before, during, and after the perfusion (scala tympani →scala vestibuli) of 50‐mM potassium perilymph. Analysis of variance and subsequent Newman‐Keuls multiple range tests were conducted on mean sample concentration values (N = 5/condition) for each of 17 endogenous amino acids. Exposure to $0.1 mM Ca+2−20 mM Mg+2$ resulted in attenuations of evoked release only for amines identified as glutamate (− 39.6%,p = 0.005) and taurine ( − 48.2%,p = 0.003). These data support the candidacy of glutamate and taurine as auditory receptoneuronal neurotransmitters or transmitter metabolites. [Supported by NIH Grants NS‐06575, NS‐16080, NS‐07058, and NSF Grant BNS‐8118772.]