Pharmacological investigation of convulsant gamma-aminobutyric acid (GABA) antagonists in amygdala-kindled rats.
The convulsant potencies of several drugs that antagonize GABAergic neurotransmission were assessed in amygdala-kindled and control rats. The potencies of picrotoxin, pentylenetetrazol, and a convulsant barbiturate were increased by amygdala kindling. No significant potentiation, however, was observed with isoniazid, 3-mercaptopropionic acid, bicuculline, or the glycine antagonist strychnine. Destruction, by electrolytic lesion, of the amygdala focus did not reverse the kindling-induced potentiation of picrotoxin convulsions. The potentiation of picrotoxin convulsions was correlated with the pattern of kindling development but not with the number of stimulations or seizures. The present results are consistent with the hypotheses that (1) kindling potentiates only some convulsant agents, (2) kindling-induced convulsant potentiation takes place outside of the kindled focus, and (3) kindling is not produced by a failure of the GABA system.
D000679:Amygdala; D000818:Animals; D003292:Convulsants / Q000494:pharmacology*; D004357:Drug Synergism; D018756:GABA Antagonists; D007696:Kindling, Neurologic / Q000187:drug effects*; D008297:Male; D010433:Pentylenetetrazole / Q000494:pharmacology; D010852:Picrotoxin / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D012640:Seizures / Q000139:chemically induced* / Q000378:metabolism; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D003292:Convulsants; D018756:GABA Antagonists; D010433:Pentylenetetrazole; D010852:Picrotoxin; D005680:gamma-Aminobutyric Acid