Abstract
Pretreatment of rats with the irreversible mu-opioid receptor antagonist, beta-funaltrexamine (beta-FNA), 20-40 mg kg-1 s.c., produced a dose-related antagonism of the reduction in respiratory rate, gastrointestinal (GI) propulsion, rotarod reaction latencies and body temperature produced by morphine administration 24 h later, suggesting that these effects are mediated via mu-opioid receptors. The kappa-receptor agonist, U-50,488H, was without effect on respiratory rate at the doses tested, but produced hypothermia, sedation and low maximum inhibition of GI propulsion. These effects of U-50,488H were not blocked by beta-FNA suggesting that they are mediated via kappa-receptors.
MeSH terms
-
3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer
-
Analgesics / toxicity*
-
Animals
-
Body Temperature / drug effects
-
Depression, Chemical
-
Dose-Response Relationship, Drug
-
Gastrointestinal Motility / drug effects
-
Hypnotics and Sedatives
-
Male
-
Morphine / antagonists & inhibitors
-
Morphine / toxicity*
-
Naltrexone / analogs & derivatives*
-
Naltrexone / pharmacology
-
Narcotic Antagonists / pharmacology*
-
Pyrrolidines / toxicity*
-
Rats
-
Rats, Inbred Strains
-
Respiration / drug effects
Substances
-
Analgesics
-
Hypnotics and Sedatives
-
Narcotic Antagonists
-
Pyrrolidines
-
Naltrexone
-
3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer
-
beta-funaltrexamine
-
Morphine