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Vol. 282, Issue 3, 1402-1407, 1997

Antisense Mapping of the MOR-1 Opioid Receptor Clone: Modulation of Hyperphagia Induced by DAMGO1

Liza Leventhal, Lesley B. Stevens, Grace C. Rossi, Gavril W. Pasternak and Richard J. Bodnar

Neuropsychology Doctoral Subprogram and Department of Psychology, Queens College, City University of New York (L.L., L.B.S., R.J.B.) and Department of NeuroOncology, Memorial Sloan-Kettering Cancer Center (G.C.R., G.W.P.), New York City, New York

The mu opioid receptor mediates ingestive behavior: mu-selective agonists stimulate food intake and antagonists reduce intake in many ingestive situations. Antisense oligodeoxynucleotides directed against each of the four exons of the MOR-1 clone were equally effective in reducing spontaneous food intake and body weight in rats. However, antisense probes directed against only exon 1 or 4 of the MOR-1 clone reduced mu-mediated analgesia. The present study examined whether central administration of antisense probes directed against each of the four exons of the MOR-1 clone or a missense control altered hyperphagia elicited by the mu agonist DAMGO across a range of doses. Antisense probes directed against only exon 1 or 4 blocked hyperphagia at agonist doses of 0.5 and 1.0 µg; this pattern was identical to that observed for mu-mediated analgesia. A missense control failed to exert significant effects, which suggests specificity of antisense actions. The effective antisense probes failed to reduce hyperphagia at a higher (5 µg) agonist dose, a result consistent with limitations in down-regulation of receptor proteins by antisense. The mu antagonist beta -funaltrexamine produced a similar pattern of effects on mu-mediated hyperphagia. The selective actions of antisense probes directed against different exons of the MOR-1 clone in reducing hyperphagia induced by DAMGO suggest that multiple splice variants of the MOR-1 clone exist and raise the possibility of further opioid receptor subclassifications.

Copyright © by The American Society for Pharmacology and Experimental Therapeutics


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