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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