CORTICOTROPIN-RELEASING FACTOR IN THE PARAVENTRICULAR NUCLEUS MODULATES FEEDING INDUCED BY NEUROPEPTIDE-Y

Central administration of neuropeptide Y (NPY) exerts a potent orexige nic effect in rats, whereas injection of corticotropin-releasing facto r (CRF) suppresses food intake. Anatomical evidence of NPY-containing terminals located in close proximity to CRF-containing neurons and ter minals of the hypothalamus and amygdala suggests possible interactions of these neuropeptide systems in food-intake regulation. The present study examined the effect of local administration of the CRF antagonis t, alpha-helical CRF9-41, or peripheral treatment with dexamethasone o n NPY-induced hyperphagia. Injection of a 250-ng dose of alpha-hel CRF within the paraventricular nucleus (PVN) of the hypothalamus signific antly potentiated the feeding induced by a 500-ng dose of NPY injected into the same locus. In contrast, feeding induced by administration o f the 500-ng dose of NPY into the ventromedial hypothalamus (VMH) was not modified by intra-VMH pre-treatment with a 250-ng dose of CRF anta gonist. No effects of NPY or alpha-hel CRF on feeding were observed af ter administration into the central nucleus of the amygdala. Systemic pre-treatment with the synthetic glucocorticoid dexamethasone at a dos e known to downregulate the function of CRF neurons in the PVN (100 mu g/kg) enhanced feeding induced by intra-PVN administration of a 500-ng dose of NPY. These results suggest that hypothalamic CRF systems in t he PVN exert inhibitory control over NPY-induced food intake.