Long-term ACTH induced diminished responsiveness of prolactin secretion to morphine.
The effect of morphine on plasma prolactin level and on dopamine turnover in the median eminence was studied using adult male rats chronically treated with ACTH. It was found that the ACTH pretreatment caused a decrease in the effect of morphine on prolactin secretion and prevented the inhibitory effect of morphine on dopamine turnover measured in the median eminence. The prolonged ACTH administration did not influence the prolactin content of the pituitaries and the in vitro dopamine sensitivity of lactotroph cells. Acute dexamethasone injection did not change the morphine-caused prolactin release. These results suggest that chronic ACTH treatment (possibly via corticosterone hyperproduction) elicits an opiate-tolerance like state of tuberoinfundibular dopaminergic neurons.
D000324:Adrenocorticotropic Hormone / Q000494:pharmacology*; D000818:Animals; D003907:Dexamethasone / Q000494:pharmacology; D004298:Dopamine / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D008297:Male; D008473:Median Eminence / Q000187:drug effects / Q000378:metabolism; D008781:Methyltyrosines / Q000494:pharmacology; D009020:Morphine / Q000494:pharmacology*; D010902:Pituitary Gland / Q000378:metabolism; D011388:Prolactin / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains
D008781:Methyltyrosines; D009020:Morphine; D003907:Dexamethasone; D000324:Adrenocorticotropic Hormone; D011388:Prolactin; D004298:Dopamine