A dual mechanism for the anticonvulsant action of aminooxyacetic acid.
The intramuscular injection of aminooxyacetic acid (AOAA) into mice elevated the concentration of gamma-aminobutyric acid (GABA) in the brain, inhibited glutamic acid decarboxylase activity and delayed the onset of isonicotinic acid hydrazide induced seizures. Analyses of these results and of those obtained previously by the authors and other workers indicated that the anticonvulsant action of AOAA involved two mechanisms. One, involving GABA metabolism, was most effective 6 h after AOAA administration, and the other, not involving GABA, was maximally effective 1.5 h after AOAA injection and was completely absent after 6 h. Depending on the convulsant agent under study, the mechanism of the anticonvulsant action of AOAA was purely of the GABA type, purely of the non-GABA type or a combination of both types.
D000085:Acetates / Q000494:pharmacology*; D000498:Allyl Compounds / Q000494:pharmacology; D000625:Aminooxyacetic Acid / Q000494:pharmacology*; D000818:Animals; D000927:Anticonvulsants; D001522:Behavior, Animal / Q000187:drug effects; D001923:Brain Chemistry / Q000187:drug effects; D004597:Electroshock; D007538:Isoniazid / Q000494:pharmacology; D008297:Male; D051379:Mice; D012640:Seizures / Q000139:chemically induced; D013997:Time Factors; D005680:gamma-Aminobutyric Acid / Q000032:analysis
D000085:Acetates; D000498:Allyl Compounds; D000927:Anticonvulsants; D000625:Aminooxyacetic Acid; D005680:gamma-Aminobutyric Acid; D007538:Isoniazid