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Abstract
Central administration of neuropeptide Y (NPY) exerts a potent orexigenic effect in
rats, whereas injection of corticotropin-releasing factor (CRF) suppresses food intake.
Anatomical evidence of NPY-containing terminals located in close proximity to CRF-containing
neurons and terminals 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 antagonist, alpha-helical CRF9-41, or
peripheral treatment with dexamethasone on NPY-induced hyperphagia. Injection of a
250-ng dose of alpha-hel CRF within the paraventricular nucleus (PVN) of the hypothalamus
significantly potentiated the feeding induced by a 500-ng dose of NPY injected into
the same locus. In contrast, feeding induced by administration of 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 antagonist. No effects of NPY or alpha-hel CRF on feeding
were observed after administration into the central nucleus of the amygdala. Systemic
pre-treatment with the synthetic glucocorticoid dexamethasone at a dose known to downregulate
the function of CRF neurons in the PVN (100 micrograms/kg) enhanced feeding induced
by intra-PVN administration of a 500-ng dose of NPY. These results suggest that hypothalamic
CRF systems in the PVN exert inhibitory control over NPY-induced food intake.