title: Dopaminergic and beta-adrenergic receptor control of alpha-melanocyte-stimulating hormone secretion during stress.
abstract: The relative roles of dopaminergic and beta-adrenergic receptors in mediating the stress-induced increase in the secretion of alpha-melanocyte-stimulating hormone (alpha-MSH) from the intermediate lobe of the pituitary were determined in the male rat. Thirty minutes of physical immobilization (restraint stress) increased the circulating concentrations of alpha-MSH and decreased the 3,4-dihydroxyphenylacetic acid/dopamine (DOPAC/DA) ratio in the intermediate lobe of the pituitary, reflecting a decrease in the tuberohypophysial dopaminergic neuronal activity. Pretreatment with the beta-adrenergic antagonist propranolol reduced the stress-induced increase in the circulating levels of alpha-MSH, but had no effect on the basal plasma concentrations of this hormone or the stress-induced decrease in DOPAC/DA in the intermediate lobe. If the dopaminergic tone during stress was maintained by administration of the DA agonist apomorphine, the stress-induced increase in alpha-MSH secretion was prevented. In nonstressed animals the administration of the beta 2-adrenergic agonist metaproterenol increased the plasma levels of alpha-MSH, and the effect of this drug was augmented if the inhibitory dopaminergic tone on alpha-MSH secretion was blocked by the administration of the DA antagonist haloperidol. Severing neurons in the retrochiasmatic region of the hypothalamus blocked the stress-induced decrease in DOPAC/DA in the intermediate lobe and attenuated the stress-induced increase in plasma concentrations of alpha-MSH. Taken together, these results indicate that a decrease in tuberohypophysial dopaminergic neuronal inhibitory tone and an increase in beta-adrenergic stimulation are both necessary for the full expression of the stress-induced increase in secretion of alpha-MSH from melanotrophs in the intermediate lobe of the rat pituitary.
authors.affiliation: Department of Pharmacology/Toxicology, Michigan State University, East Lansing.
authors.forename: S E
authors.initials: SE
authors.lastname: Lindley
authors.forename: K J
authors.initials: KJ
authors.lastname: Lookingland
authors.forename: K E
authors.initials: KE
authors.lastname: Moore
mesh_terms: D000344:Afferent Pathways / Q000502:physiology; D000818:Animals; D001058:Apomorphine / Q000494:pharmacology; D003714:Denervation; D004357:Drug Synergism; D006220:Haloperidol / Q000494:pharmacology; D007033:Hypothalamus, Middle / Q000502:physiology; D066298:In Vitro Techniques; D008297:Male; D009921:Metaproterenol / Q000494:pharmacology; D010902:Pituitary Gland / Q000378:metabolism; D011433:Propranolol / Q000494:pharmacology; D011863:Radioimmunoassay; D051381:Rats; D011943:Receptors, Adrenergic, beta / Q000187:drug effects / Q000502:physiology*; D011954:Receptors, Dopamine / Q000187:drug effects / Q000502:physiology*; D013315:Stress, Psychological / Q000378:metabolism*; D000521:alpha-MSH / Q000378:metabolism*
chemical_list: D011943:Receptors, Adrenergic, beta; D011954:Receptors, Dopamine; D009921:Metaproterenol; D000521:alpha-MSH; D011433:Propranolol; D006220:Haloperidol; D001058:Apomorphine