[Adrenocorticotropic hormone (ACTH): antagonistic effect on opioid analgesia in central nervous system of the rat and its possible mechanisms of action].
Using the behavioral pharmacological approach, we have studied the influence of ACTH on the analgesia mediated by three types of opioid receptors (mu, delta, kappa). The mechanisms by which ACTH antagonizes opioid analgesia were explored at receptor level and post-receptor second messenger level. The expression of Fos protein induced by ACTH was also observed in rat brain. The main results show that ACTH selectively antagonizes spinal opioid analgesia mediated by mu and delta, but not kappa receptors. The proposed mechanisms of the anti-opioid effect of ACTH are that ACTH can modulate opioid-induced decrease of intracellular cAMP content and the suppression of calcium influx. ACTH has been shown to induce Fos protein expression in selected brain areas including the nuclei involved in pain modulation. These brain areas may serve as sites of action for ACTH to exert its anti-opioid effect.
Fang
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Department of Physiology, Beijing Medical University.
D018712:Analgesics, Non-Narcotic / Q000037:antagonists & inhibitors; D000701:Analgesics, Opioid / Q000037:antagonists & inhibitors; D000818:Animals; D001921:Brain / Q000378:metabolism*; D003366:Cosyntropin / Q000494:pharmacology*; D000242:Cyclic AMP / Q000378:metabolism; D017288:Pain Threshold / Q000187:drug effects*; D016760:Proto-Oncogene Proteins c-fos / Q000096:biosynthesis; D051381:Rats; D011957:Receptors, Opioid / Q000502:physiology
D018712:Analgesics, Non-Narcotic; D000701:Analgesics, Opioid; D016760:Proto-Oncogene Proteins c-fos; D011957:Receptors, Opioid; D003366:Cosyntropin; D000242:Cyclic AMP