Involvement of GABA in the antinociceptive effect of gamma-acetylenic GABA (GAG), an inhibitor of GABA-transaminase.
The role of both novel GABAB and classical GABAA receptors in GAG-induced anti-nociception was investigated using the tail flick and hot plate tests. To this end, manipulations known to increase baclofen-induced antinociception (GABAB) and the receptor antagonist bicuculline (GABAA) were used. Of the modifiers of monoamine function tested, only chlorpromazine and haloperidol significantly increased GAG-induced antinociception. Theophylline antagonized antinociception produced by both GAG and GVG. Bicuculline did not antagonize antinociception produced by either GAG or muscimol. GAG-induced antinociception does not appear to result from the activation of either classical or novel GABA receptors. An interaction with dopaminergic pathways appears to be involved.
D000612:4-Aminobutyrate Transaminase / Q000037:antagonists & inhibitors*; D000480:Alkynes; D000614:Aminocaproates / Q000494:pharmacology*; D000700:Analgesics; D000818:Animals; D001418:Baclofen / Q000494:pharmacology; D001640:Bicuculline / Q000494:pharmacology; D004347:Drug Interactions; D008297:Male; D009118:Muscimol / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D013806:Theophylline / Q000494:pharmacology; D013997:Time Factors; D005680:gamma-Aminobutyric Acid / Q000502:physiology*
D000480:Alkynes; D000614:Aminocaproates; D000700:Analgesics; D009118:Muscimol; D005680:gamma-Aminobutyric Acid; C013785:4-amino-5-hexynoic acid; D013806:Theophylline; D000612:4-Aminobutyrate Transaminase; D001418:Baclofen; D001640:Bicuculline