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.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Eating / drug effects
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Exons
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Hyperphagia / chemically induced
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Hyperphagia / physiopathology*
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Male
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Naltrexone / pharmacology
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Narcotic Antagonists / pharmacology
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Nociceptin
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Nociceptin Receptor
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Oligonucleotides, Antisense / pharmacology*
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Opioid Peptides / toxicity*
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Rats
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Rats, Sprague-Dawley
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Receptors, Opioid / genetics
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Receptors, Opioid / physiology*
Substances
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Narcotic Antagonists
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Oligonucleotides, Antisense
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Opioid Peptides
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Receptors, Opioid
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Naltrexone
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Nociceptin Receptor
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Oprl protein, rat