The opiate antagonist naloxone was used to examine the possibility that endogenous opioid function is involved in the expression of the increased feeding observed following intracerebroventricular (i.c.v.) administration of rat hypothalamic growth hormone-releasing factor (GRF). It was found that systemically administered naloxone (0.125, 0.25 and 0.50 mg/kg) significantly suppressed the increased food intake observed following i.c.v. GRF (4.0 pmol) treatment. Though potent enough to eliminate ingestive effects of GRF, baseline food intake was unaffected by 0.125 mg/kg naloxone. Examination of 0.4, 4.0 and 40.0 pmol i.c.v. administered GRF-(3-40), a structurally related but physiologically inactive peptide, revealed no effect on food intake. The present results suggest involvement of endogenous opioid function in GRF-stimulated feeding.
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