Opioid receptor involvement in food deprivation-induced feeding: Evaluation of selective antagonist and antisense oligodeoxynucleotide probe effects in mice and rats

M. M. Hadjimarkou, A. Singh, Y. Kandov, Y. Israel, Y. X. Pan, G. C. Rossi, G. W. Pasternak, Richard J. Bodnar

Research output: Contribution to journalArticlepeer-review

Abstract

Central administration of general and selective opioid receptor subtype antagonists in the rat has revealed a substantial role for μ, a moderate role for κ, and a minimal role for δ receptors in the mediation of deprivation-induced feeding. Antisense probes directed against the κ opioid receptor (KOP), nociceptin opioid receptor (NOP), and δ opioid receptor (DOP) genes in rats result in reductions similar to κ and δ antagonists, whereas antisense probes directed against the μ opioid receptor (MOP) gene produced modest reductions relative to μ antagonists, suggesting that isoforms of the MOP gene may mediate deprivation-induced feeding. Since these isoforms were initially identified in mice, the present study compared the effects of general and selective opioid receptor antagonists on deprivation-induced feeding in rats and mice and antisense probes directed against exons of the MOP, DOP, KOP, and NOP genes on deprivation-induced feeding in the mouse, Food-deprived (12 and 24 h) rats and mice displayed similar profiles of reductions in deprivation-induced feeding following general, μ, and κ opioid antagonists. In contrast, mice, but not rats, displayed reductions in deprivation-induced intake following δ antagonism as well as DOP antisense probes, suggesting a species-specific role for the δ receptor. Antisense probes directed against the KOP and NOP genes also reduced deprivation-induced intake in mice in a manner similar to κ antagonism. However, the significant reductions in deprivation - induced feeding following antisense probes directed against either exons 2, 4, 7, 8, or 13 of the MOP gene were modest compared with μ antagonism, suggesting a role for multiple A-mediated mechanisms.

Original languageEnglish
Pages (from-to)1188-1202
Number of pages15
JournalJournal of Pharmacology and Experimental Therapeutics
Volume311
Issue number3
DOIs
Publication statusPublished - Dec 2004

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