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GAMMA‐HYDROXYBUTYRATE DEGRADATION IN THE BRAIN IN VIVO : NEGLIGIBLE DIRECT CONVERSION TO GABA
Author(s) -
Möhler H.,
Patel A. J.,
Balázs R.
Publication year - 1976
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.1471-4159.1976.tb01572.x
Subject(s) - tricarboxylic acid , citric acid cycle , glutamine , glutamate receptor , metabolism , in vivo , chemistry , biochemistry , gamma hydroxybutyrate , amino acid , biology , pharmacology , receptor , microbiology and biotechnology
— The metabolism of γ‐hydroxybutyrate (GHB) was studied by following the fate of [1‐ 14 C]GHB in mouse brain after an intravenous injection. Cerebral uptake of GHB was rapid and this substance disappeared from brain tissue with a half‐life of approx 5 min. Degradation of [1‐ 14 C]GHB took place in the brain since 14 C was incorporated in amino acids associated with the tricarboxylic acid cycle: the labelling pattern was consistent with the oxidation of GHB via succinate through the cycle, rather than with β‐oxidation of GHB. Conversion of [ 14 C]GHB into [ 14 C]GABA prior to oxidation was negligible, thus it is unlikely that the pharmacological action of GHB would be mediated through GABA formation. [ 14 C]GHB oxidation also elicited the signs of metabolic compartmentation of the tricarboxylic acid cycle in the brain (glutamine/glutamate specific radioactivity ratio was about 4).