Plasma corticosterone changes in response to central or peripheral administration of kappa and sigma opiate agonists.
The acute administration of morphine produces a characteristic increase in plasma corticosterone. By using the male rat with a chronic i.v. catheter, a stereotaxically placed cannula in the lateral ventricle and a sound-attenuated one-way vision chamber, the effects of prototypic kappa and sigma opiate receptor agonists were studied. Both ethyl-ketocyclazocine (EKC) and N-allyl-normetazocine [SKF 10047] (SKF) also produced such a rise in hormone level after i.v. or i.c.v. administration. The former effect was blocked by concurrent treatment with naloxone (NX), 0.4 mg/kg. The latter effect was not blocked by i.c.v. pretreatment with beta-funaltrexamine, a long-acting mu receptor antagonist, whereas the response to i.c.v. morphine was attenuated significantly. The development of acute dependence and short-term tolerance to EKC and SKF was also studied. Priming with either drug (i.v.) did not result in a NX-precipitated plasma corticosterone withdrawal response 3 hr later. Similar studies priming with morphine (i.c.v.) did result in the plasma corticosterone-elevated response when NX was administered i.c.v. after 3 hr. When EKC or SKF was substituted for morphine, no NX-induced response was observed. Short-term tolerance to the effects of EKC and SKF on the hypothalamo-pituitary-adrenal axis did not appear to occur. These data support the notion that stimulation of several subclasses of opiate receptors will result in the activation of the hypothalamo-pituitary-adrenal axis. Furthermore, it appears that the mu opiate receptor is involved in the initiation of acute opiate dependence.
Eisenberg
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D000818:Animals; D001921:Brain / Q000187:drug effects*; D003345:Corticosterone / Q000097:blood*; D003496:Cyclazocine / Q000031:analogs & derivatives / Q000494:pharmacology; D016314:Ethylketocyclazocine; D006801:Humans; D007030:Hypothalamo-Hypophyseal System / Q000187:drug effects; D008297:Male; D009020:Morphine / Q000494:pharmacology; D009270:Naloxone / Q000494:pharmacology; D009271:Naltrexone / Q000031:analogs & derivatives / Q000494:pharmacology; D009293:Opioid-Related Disorders; D010620:Phenazocine / Q000031:analogs & derivatives / Q000494:pharmacology; D010913:Pituitary-Adrenal System / Q000187:drug effects; D051381:Rats; D011919:Rats, Inbred Strains; D011957:Receptors, Opioid / Q000187:drug effects* / Q000502:physiology; D017473:Receptors, Opioid, kappa; D017450:Receptors, Opioid, mu; D017480:Receptors, sigma
D011957:Receptors, Opioid; D017473:Receptors, Opioid, kappa; D017450:Receptors, Opioid, mu; D017480:Receptors, sigma; D009270:Naloxone; D016314:Ethylketocyclazocine; D009271:Naltrexone; C024524:beta-funaltrexamine; C012134:SK&F 10047; D009020:Morphine; D010620:Phenazocine; D003496:Cyclazocine; D003345:Corticosterone