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VP Bakshi and AE Kelley
Department of Psychology, Northeastern University, Boston, Massachusetts.
Previous work has shown that morphine infusion into the ventral striatum results in marked hyperphagia in satiated rats. The present investigation was undertaken to determine the relative involvement of opiate receptor subtypes in this phenomenon. Equimolar doses of the synthetic ligands [D-Ala2,NME-Phe4,Gly-ol5]-enkephalin (DAMGO; 0, 0.025, 0.25, and 2.5 micrograms/0.5 microliter), [D-Pen2,5]-enkephalin (DPEN; 0, 0.031, 0.31, 3.1 and 6.2 micrograms/0.5 microliter) and U50,488H (0, 0.0186, 0.186, 1.86 and 3.72 micrograms/0.5 microliters), which are selective for mu, delta and kappa receptors, respectively, were microinfused into three striatal sites: the nucleus accumbens, ventromedial striatum and ventrolateral striatum. Food intake (grams), feeding, drinking, locomotion, rearing and grooming were measured. After injection into all three sites, DAMGO induced a robust, dose- dependent increase in food intake that was blocked by coadministration of naltrexone (5 mg/kg i.p.). DAMGO-induced feeding was delayed in onset and was long lasting. Injections of DPEN were 2 to 3 times less effective in eliciting feeding. DPEN-induced feeding occurred immediately and was short lasting. U50,488H had no effect on food intake. No changes in drinking were noted for any agonist. Spontaneous motor behaviors were also increased by DAMGO and DPEN. These findings demonstrate that mu opiate receptors within the ventral striatum mediate the opiate-induced feeding response.
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