The effect of cochlear nerve lesion on the release of glutamate, aspartate, and GABA from cat cochlear nucleus, in vitro.

Abstract

Pool studies of glutamate and aspartate have suggested a transmitter role for these amino acids in cochlear nerve endings. As further evidence. the K+-evoked release of glutamate, aspartate and GABA was measured in cat cochlear nucleus slices in vitro and compared to the release following a cochlear nerve lesion. Using [3H]glutamine as precursor, the K+-evoked release of glutamate and γ-aminobutyric acid (GABA) was respectively 4.1 and 7.2 times the spontaneous release. Using [14C]glutamate as a marker, the K+-evoked release of glutamate and GABA was respectively 7.1 and 2.8 times the basal release. All K+-evoked releases were Ca++-dependent. Nine days after unilateral lesion of the cochlear nerve in the cat, the glutamate release decreased by about 75% on the lesioned side compared to the intact one, whereas the GABA release was not decreased. The labelled tissue glutamate, either synthesized from [3H]glutamine or labelled with [14C]glutamate, was also markedly decreased on the lesioned side. In comparison, the evoked release of aspartate, newly synthesized from [14C]glutamate, remained low and was only decreased by about 45% after cochlear nerve lesions. Comparing cat with rat cochlear nucleus, the glutamate release was similar in both animals, whereas the GABA release was much higher in the rat. It is concluded that glutamate and to a lesser extent aspartate are likely to be released from cochlear nerve terminals, supporting a transmitter role in these nerve fibres for both amino acids.