© Elsevier/North-Holland Biomedical Press An inability of 7-acetylenic GABA to block eating evoked by hypothalamic stimulation

Several ines 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,},-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 hreshold for evoking eating by ESLH. Implications of results for understanding mechanisms underlying ESLH-induced eating are discussed. Although it has been known for over 20 years that hypothalamic stimu-lation may evoke ating in satiated animals [10], the mechanisms underlying this fascinating phenomenon remain unclear. A number of investigators have argued that he eating observed uring electrical stimulation of the lateral hypothalamus (ESLH) results from activation of specific neural circuits regulating hunger [7, 16]. In contrast, Valenstein and hi. ~ colleagues have demonstrated that the eating and other behaviors evoked by ESLH are much more stereotyped, an