An inability of gamma-acetylenic GABA to block eating evoked by hypothalamic stimulation.
Several lines of evidence have implicated the nigrostriatal dopamine system and the neocortex for eating occurring either spontaneously or in response to electrical stimulation of the lateral hypothalamus (ESLH). GABA-ergic neural systems are known to modulate activity in the nigrostriatal system and neocortex. The GABA-transaminase inhibitor, gamma-acetylenic GABA (GAG) was administered to rats eating in response to ESLH. This drug produced hypersynchronization of the cortical EEG and behavioral sedation, but did not alter the current threshold for evoking eating by ESLH. Implications of results for understanding mechanisms underlying ESLH-induced eating are discussed.
D000480:Alkynes; D000614:Aminocaproates / Q000494:pharmacology*; D000818:Animals; D001835:Body Weight; D001923:Brain Chemistry / Q000187:drug effects; D004558:Electric Stimulation; D005247:Feeding Behavior / Q000187:drug effects*; D007031:Hypothalamus / Q000502:physiology*; D007033:Hypothalamus, Middle / Q000502:physiology; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D000480:Alkynes; D000614:Aminocaproates; D005680:gamma-Aminobutyric Acid; C013785:4-amino-5-hexynoic acid