Lesions of the posterior basolateral amygdala block feeding induced by systemic 8-OH-DPAT.

We have recently reported that bilateral electrolytic lesions of the posterodorsal amygdala (PDA) in female rats which induce protracted overeating and weight gain also attenuate short-term feeding stimulated by intraraphe infusions of the serotonin (5-HT) 1A agonist, (+/-)-8-hydroxy-2-(di-n-propylamino)tetralin, (8-OH-DPAT). Bilateral lesions of the posterior basolateral amygdala (pBLA) in male rats have also been reported to enhance feeding and weight gain, but much less so than PDA lesions do in female rats. The present study was performed to determine if pBLA lesions in female rats might attenuate 8-OH-DPAT feeding and what, if any, relationship exists between 8-OH-DPAT-induced feeding and lesion-induced weight gain. Lesioned rats showed reliable increases in 24-h food intake and weight gain relative to shams during the days between surgery and acute drug-induced feeding tests. 8-OH-DPAT (0, 60, 120 or 240 microg/kg in saline) increased feeding of shams in a dose-dependent manner over 2 h. Feeding at the most effective dose (120 microg/kg) was reduced to vehicle levels in lesioned rats. The feeding induced by this dose correlated inversely (r=-.59, P<.01) with the magnitude of weight gained following lesions. Feeding at the highest dose (240 microg/kg) showed a biphasic effect of feeding inhibition over the first vs. second hour that was unaffected by lesions. These findings imply that either fibers of passage and/or cellular elements in both the PDA and pBLA normally inhibit overeating and weight gain via intact serotonergic mechanisms.