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Alteration in Neuronal‐Glial Metabolism of Glutamate by the Neurotoxin Kainic Acid
Author(s) -
Krespan Barbara,
Berl Soil,
Nicklas William J.
Publication year - 1982
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1982.tb08657.x
Subject(s) - kainic acid , glutamate receptor , glutamine , biochemistry , cerebellum , neurotoxin , chemistry , glutamic acid , glutamine synthetase , veratridine , biology , endocrinology , amino acid , sodium , organic chemistry , receptor , sodium channel
The effect of the excitotoxin kainic acid on glutamate and glutamine metabolism was studied in cerebellar slices incubated with d ‐[2‐ 14 C]glucose, [U‐ 14 C]‐γ‐aminobutyric acid, [ 3 H]acetate, [U‐ 14 C]glutamate, and [U‐ 14 C]glutamine as precursors. Kainic acid (1 m m ) strongly inhibited the labeling of glutamine relative to that of glutamate from all precursors except [2‐ 14 C]glucose and [U‐ 14 C]glutamine. Kainic acid did not inhibit glutamine synthetase directly. The data indicate that in the cerebellum kainic acid inhibits the synthesis of glutamine from the small pool of glutamate that is thought to be associated with glial cells. Kainic acid also markedly stimulated the efflux of glutamate from cerebellar slices and this release was not sensitive to tetrodotox‐in. Kainic acid stimulated efflux of both glucose‐and acetate‐labeled glutamate. In contrast, veratridine released glucose‐labeled glutamate preferentially via a tetrodotoxin‐sensitive mechanism. Kainic acid did not release [U‐ 14 C]glutamate from synaptosomal fractions. These results suggest that the bulk of the glutamate released from cerebellar slices by kainic acid comes from nonsynaptic pools.