Abstract
We studied the effect of the mu antagonist, beta-funaltrexamine (beta-FNA) on deprivation and opioid-induced feeding. Intracerebroventricular pre-treatment of 20 h deprived rats with 0.1, 1, 10 and 20 nmol of beta-FNA decreased feeding by 24%, 50%, 50% and 38% during the first hour. Central administration of beta-FNA (0.1, 1 and 10 nmol) also decreased feeding induced by the mu opioid agonist, DAMGO by 57%, 60% and 71%. Feeding induced by the delta agonist, DSLET, was decreased by pre-treatment with beta-FNA; but only during the 1-2 h time points, a time when relatively little food was ingested. Intraventricular injection of beta-FNA failed to alter feeding stimulated by the kappa opioid agonist, U-50,488H. These data further substantiate a role for the opioid receptor in deprivation and opioid-induced feeding.
Publication types
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Research Support, U.S. Gov't, Non-P.H.S.
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer
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Animals
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Enkephalin, Ala(2)-MePhe(4)-Gly(5)-
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Enkephalins / pharmacology*
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Feeding Behavior / drug effects*
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Food Deprivation / physiology*
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Injections, Intraventricular
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Male
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Naltrexone / analogs & derivatives*
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Naltrexone / pharmacology
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Narcotic Antagonists / pharmacology*
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Pyrrolidines / pharmacology
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Rats
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Rats, Inbred Strains
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Receptors, Opioid / drug effects
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Receptors, Opioid, kappa
Substances
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Enkephalins
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Narcotic Antagonists
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Pyrrolidines
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Receptors, Opioid
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Receptors, Opioid, kappa
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Enkephalin, Ala(2)-MePhe(4)-Gly(5)-
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Naltrexone
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3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer
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beta-funaltrexamine