Abstract
Rats with dorsomedial hypothalamic lesions (DMN-L) or sham operations were injected IP with saline or the satiety peptide cholecystokinin (CCK) at 3.0 and 6.0 μg/kg at the onset of the dark phase. Food consumption was then measured 15, 30 and 60 min later. Compared to saline baseline intake. CCK suppressed feeding during the first 30 min following injection in the sham operated group but not in the DMN-L group. Bombesin (BBS), another satiety peptide was also injected (4.0 and 8.0 μg/kg) into the two groups. BBS produced significant and comparable suppression of feeding in both DMN-L and sham operated rats. In a third trial a large dose of CCK (12.0 μg/kg) was injected into the two groups as described above. The CCK suppressed feeding for 60 min in the control group. CCK also attenuated feeding in the DMN-L group, but for only 30 min. However, even this suppression was reduced compared to the control group. The data suggest that the DMN may play a role in CCK induced satiety.
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