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Orphan opioid receptor antisense probes block orphanin FQ-induced hyperphagia.

Abstract
Orphanin FQ/nociceptin binds with high affinity to the orphan opioid receptor-like/K-3 (ORL1/KOR-3) clone, and stimulates feeding. The present study demonstrated that antisense oligodeoxynucleotides directed against either exons 1, 2 or 3 of the ORL1/KOR-3 clone reduced orphanin FQ/nociceptin-induced hyperphagia. A missense probe was ineffective. Naltrexone dose-dependently reduced orphanin FQ/nociceptin-induced hyperphagia. These data suggest that the receptor responsible for orphanin FQ/nociceptin-induced hyperphagia is encoded by the ORL1/KOR-3 clone.
AuthorsL Leventhal, J P Mathis, G C Rossi, G W Pasternak, R J Bodnar
JournalEuropean journal of pharmacology (Eur J Pharmacol) Vol. 349 Issue 1 Pg. R1-3 (May 15 1998) ISSN: 0014-2999 [Print] Netherlands
PMID9669488 (Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)
Chemical References
  • Narcotic Antagonists
  • Oligonucleotides, Antisense
  • Opioid Peptides
  • Receptors, Opioid
  • Naltrexone
  • nociceptin
  • Nociceptin Receptor
  • Oprl protein, rat
Topics
  • Animals
  • Eating (drug effects)
  • Exons
  • Hyperphagia (chemically induced, physiopathology)
  • Male
  • Naltrexone (pharmacology)
  • Narcotic Antagonists (pharmacology)
  • Oligonucleotides, Antisense (pharmacology)
  • Opioid Peptides (toxicity)
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, Opioid (genetics, physiology)
  • Nociceptin Receptor

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