Abstract

Expression of CART (cocaine–amphetamine-regulated transcript) in the rat hypothalamus is modulated by nutritional status, and injection of synthetic CART peptide into the forebrain ventricular system suppresses food intake, indicating a possible role in hypothalamic control of energy homeostasis. Its recent identification in cell bodies and central terminals of vagal afferent neurons additionally suggests a role in brainstem mechanisms of meal termination and satiety. We demonstrate here that CART[55–102] (0.2 nmol) suppresses short-term sucrose intake and overnight chow intake in non-food-deprived rats even more when delivered into the fourth ventricle as compared to the lateral ventricle. At the threshold dose (0.02–0.08 nmol) no readily noticeable motor impairments were observed. The results are consistent, but do not prove a site of action within the brainstem, possibly in mediating vagal satiety signals at the level of the NTS.

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