Maturation of the prolactin and proopiomelanocortin-derived peptide responses to ether stress and morphine: neurochemical analysis.
The hormonal and neurochemical responses to acute ether stress, morphine, and/or naloxone were analyzed in infantile (13-day-old) and prepubertal (36-day-old) male CD rats in an attempt to identify a possible neurochemical correlate(s) for the previously demonstrated requisite maturation of the PRL response to ether stress. Neuronal serotonin (5-HT), norepinephrine (NE), and dopamine (DA) activities were examined in the medial preoptic hypothalamic area (MPOH), medial basal hypothalamic area (MBH), and median eminence (ME). Ether stress increased plasma PRL, ACTH, and beta-endorphin-like immunoreactivity (beta end) as well as NE metabolism in the MPOH and MBH and neuronal 5-HT activity in the MBH, and decreased neuronal DA activity in the ME of prepubertal animals. Ether stress elicited similar changes in infantile animals, with the important exceptions that plasma PRL, neuronal 5-HT activity in the MBH, and neuronal DA synthesis in the ME were not affected at this earlier age. Morphine increased plasma PRL, ACTH, and beta end levels, elevated neuronal NE and 5-HT activities in the MPOH and MBH, and decreased DA synthesis in the ME in both infantile and prepubertal animals. Naloxone administration did not alter basal hormone concentrations or neuronal monoamine activity in any brain area, but did prevent all of the morphine-induced changes as well as the ether stress-induced changes in PRL, MBH neuronal 5-HT activity, and DA synthesis in the ME of prepubertal animals. In addition, naloxone augmented the ether stress-induced increases in ACTH and beta end in prepubertal rats. Indirect stimulation of 5-HT neurons by administration of the amino acid precursor of 5-HT, 5-hydroxytryptophan, resulted in decreased DA synthesis in the ME of infantile animals and increased plasma PRL levels in that age group, indicating that this portion of the neurochemical connection is already present in infantile animals. Furthermore, the 5-hydroxytryptophan-induced increase in PRL was blocked by pretreatment with naloxone. The results demonstrate that both the ether stress- and morphine-induced increases in plasma PRL, but not in ACTH or beta end, are associated with increased neuronal 5-HT activity in the MBH and a decreased neuronal DA activity in the ME, that these are opiate receptor-mediated effects, and that infantile rats apparently lack a functional opiate-5-HT connection, which matures some time between days 13 and 36 postnatally.
D006916:5-Hydroxytryptophan / Q000494:pharmacology; D000324:Adrenocorticotropic Hormone / Q000097:blood; D000375:Aging; D000818:Animals; D000831:Animals, Newborn / Q000378:metabolism; D004298:Dopamine / Q000378:metabolism; D004723:Endorphins / Q000097:blood; D004986:Ether; D007033:Hypothalamus, Middle / Q000254:growth & development / Q000378:metabolism; D008297:Male; D008473:Median Eminence / Q000254:growth & development / Q000378:metabolism; D009020:Morphine / Q000494:pharmacology*; D009474:Neurons / Q000187:drug effects / Q000378:metabolism; D009638:Norepinephrine / Q000378:metabolism; D011301:Preoptic Area / Q000254:growth & development / Q000378:metabolism; D011333:Pro-Opiomelanocortin / Q000378:metabolism*; D011388:Prolactin / Q000097:blood / Q000378:metabolism*; D051381:Rats; D012701:Serotonin / Q000378:metabolism; D012741:Sexual Maturation; D013312:Stress, Physiological / Q000139:chemically induced / Q000378:metabolism*; D001615:beta-Endorphin
D004723:Endorphins; D004986:Ether; D012701:Serotonin; D001615:beta-Endorphin; D011333:Pro-Opiomelanocortin; D009020:Morphine; D000324:Adrenocorticotropic Hormone; D011388:Prolactin; D006916:5-Hydroxytryptophan; D004298:Dopamine; D009638:Norepinephrine