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AMMONIUM ION INHIBITION OF EVOKED RELEASE OF ENDOGENOUS GLUTAMATE FROM HIPPOCAMPAL SLICES
Author(s) -
Hamberger Anders,
Hedquist Bo,
Nyström Britta
Publication year - 1979
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.1471-4159.1979.tb05276.x
Subject(s) - glutamate receptor , ammonium chloride , endogeny , ammonium , glutamine , incubation , efflux , hippocampal formation , depolarization , chemistry , metabolism , biophysics , biochemistry , biology , endocrinology , medicine , amino acid , receptor , organic chemistry
— The effect of pathophysiological levels (2‐5 m m ) of ammonium chloride on the efflux of endogenous and exogenous [ 14 C]glutamate from hippocampal slices was studied. The evoked release of glutamate which occurs dring tissue depolarization with 56 m m ‐KCl was greatly reduced when the tissue had been exposed to NH 4 Cl for 40–80 min. This effect was seen whether or not glutamine (0.5 m m ) was present in the incubation medium. The effect was completely reversible. The spontaneous efflux and the evoked release of [ 14 C]glutamate was, on the contrary, completely unaltered after exposure of the slice to ammonium ions. Nigher (20–36 m m ) amounts of NH 4 Cl evoked a release of [ 14 C]glutamate from the crude mitochondrial fraction, as did high concentrations of KCl. The results are discussed in relation to the compartmentation of glutamate metabolism and the pathogenesis of hepatic coma.