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A Regional Study of 4‐Aminobutyrate Metabolism and Amino Acid Levels in Rat Brain Following Chronic Oral Administration of Ethanolamine O ‐Sulphate
Author(s) -
Fletcher Allan,
Fowler Leslie 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.tb05343.x
Subject(s) - glutamate decarboxylase , medicine , gaba transaminase , endocrinology , chemistry , glutamine , neurochemical , glutamine synthetase , amino acid , striatum , glutamate receptor , metabolism , transaminase , cerebellum , ethanolamine , biochemistry , enzyme , biology , dopamine , receptor
Ethanolamine O‐sulphate (EOS) dissolved in the drinking water (5mg‐ml −1 ) was administered ad libitum to rats for 26 days. At the end of this period, glutamate decarboxylase (GAD) and GABA‐transaminase (GABA‐T) activities, 4‐aminobutyrate (GABA) concentration, and the levels of six other amino acids were measured in various brain regions. Significant inhibition of GABA‐T accompanied by significant increases in GABA content were observed throughout the brain, although the magnitudes of these effects varied according to region. GAD activity was significantly reduced in most brain regions, although this effect was apparently not related to cofactor availability or the direct actions of EOS or increased GABA concentration. Glutamine levels were significantly reduced to approximately 72% of control values in all brain regions. Aspartate levels were significantly reduced to approximately 84% of control values in all regions except the striatum and cerebellum. Minor changes in other amino acid levels were also detected. These neurochemical changes which accompanied the primary effect of EOS on GABA‐T are discussed in terms of indirect secondary metabolic changes rather than nonspecific enzyme inhibition by EOS.