Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P80404 (GABA transaminase)
 786 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two clinically effective anticonvulsants, phenobarbitone and diazepam, protected 5-day old chicks against picrotoxin convulsions without reducing brain GABA-transaminase activity or raising brain GABA concentration. Ethanolamine-O-sulphate and amino-oxyacetic acid, in doses which inhibited GABA-transminase by at least 63% and approximately doubled brain GABA concentration, did not significantly affect the ED50 for picrotoxin convulsions. The ED50 for picrotoxin convulsions was significantly raised by di-n-propylacetate (800 mg/kg) which inhibited GABA transaminase activity by 6% and elevated brain GABA concentration by 26%.
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PMID:Picrotoxin convulsions and GABA metabolism after injection of anticonvulsants in chicks. 99 20

2-Aminoethanol (ethanolamine) was studied for effects on neurochemical assays for GABA synthesis, receptor binding, uptake and metabolism in rat brain preparations. The effects of ethanolamine were compared with those of ethanolamine O-sulphate (EOS), an inhibitor of GABA degradation. Furthermore, the effect of both compounds was compared on GABA metabolism in rat brain in vivo. In vitro, ethanolamine and EOS had no significant effect on the GABA synthesizing enzyme glutamic decarboxylase (GAD) and GABA uptake, but both drugs proved virtually equipotent to inhibit the GABA degrading enzyme GABA aminotransferase (GABA-T). EOS was a relatively potent inhibitor of GABA receptor binding, whereas ethanolamine was not effective in this regard. Following systemic administration in rats, 50% inhibition of GABA-T in the brain was achieved by 500 mg/kg ethanolamine or 2000 mg/kg EOS, respectively. As a consequence of GABA-T inhibition, GABA levels increased significantly. GAD activity remained unchanged after both treatments. The present results suggest that the recently reported enhancement of functional effects of GABA by ethanolamine may relate, at least in part, to the inhibitory effect of the compound on GABA catabolism.
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PMID:Effect of 2-aminoethanol on the synthesis, binding, uptake and metabolism of GABA. 632 73

Ethanolamine O-sulphate (EOS) dissolved in the drinking water (5 mg . ml(-1) was administered ad libitum to rats for 26 days. At the end of this period, glutamate decarboxylase (GAD) and GAA-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.
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PMID:A regional study of 4-aminobutyrate metabolism and amino acid levels in rat brain following chronic oral administration of ethanolamine O-sulphate. 706 27