title: Lack of effect of prolactin on the dopaminergic receptor sensitivity in striatal and limbic areas after experimentally-induced alterations in its peripheral levels.
abstract: Although it had been suggested that prolactin (PRL) modulates the dopaminergic receptor sensitivity in extrahypothalamic areas, recent studies have questioned this role. We studied the effects of PRL on the receptor sensitivity in the striatum and the limbic forebrain, analyzing the number of D1 and D2 receptors and the amount of their second messenger, cyclic-adenosine monophosphate (cAMP). Tyrosine hydroxylase (TH) activity and dopamine (DA) and L-3,4-dihydroxyphenylacetic acid (DOPAC) content were also measured as indices of presynaptic activity. The study was carried out in male rats submitted to either acute (PRL injection) or chronic (pituitary grafts or diethylstilbestrol (DES)-induced pituitary tumors) rises of plasma PRL levels. The results showed a common lack of effect of PRL on the dopaminergic receptor sensitivity in both brain areas and, only some few effects on presynaptic activity in the striatum. Thus, grafted rats showed a slight decrease in DA content in the striatum, but neither D1 and D2 receptor number and cAMP content nor DOPAC content and TH activity, were modified, whereas DES animals exhibited no changes in all the parameters studied. A single injection of ovine PRL caused a decrease in DOPAC content and an increase in TH activity in the striatum. In the case of the limbic area, both chronic and acute hyperprolactinemia failed to alter any of the indices studied. In summary, we cannot support the view that PRL plays a role as modulator of dopaminergic receptor sensitivity. The only effects were always produced at the presynaptic level on the striatum, and after acute treatment, which supports the possible development of tolerance after chronic changes in peripheral PRL levels.
authors.affiliation: Department of Biochemistry, Faculty of Medicine, Complutense University, Madrid, Spain.
authors.forename: M
authors.initials: M
authors.lastname: Cebeira
authors.forename: M L
authors.initials: ML
authors.lastname: Hernandez
authors.forename: F
authors.initials: F
authors.lastname: Rodriguez de Fonseca
authors.forename: R
authors.initials: R
authors.lastname: de Miguel
authors.forename: J J
authors.initials: JJ
authors.lastname: Fernandez-Ruiz
authors.forename: J A
authors.initials: JA
authors.lastname: Ramos
mesh_terms: D015102:3,4-Dihydroxyphenylacetic Acid / Q000378:metabolism; D000818:Animals; D001921:Brain / Q000378:metabolism*; D003342:Corpus Striatum / Q000378:metabolism*; D000242:Cyclic AMP / Q000378:metabolism; D004054:Diethylstilbestrol / Q000494:pharmacology; D004298:Dopamine / Q000378:metabolism; D004343:Drug Implants; D005260:Female; D008032:Limbic System / Q000378:metabolism*; D008297:Male; D010903:Pituitary Gland, Anterior / Q000378:metabolism / Q000601:surgery; D010911:Pituitary Neoplasms / Q000139:chemically induced / Q000503:physiopathology; D011388:Prolactin / Q000097:blood / Q000378:metabolism / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains; D011954:Receptors, Dopamine / Q000187:drug effects / Q000378:metabolism*; D017447:Receptors, Dopamine D1; D017448:Receptors, Dopamine D2; D012016:Reference Values; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism
chemical_list: D004343:Drug Implants; D011954:Receptors, Dopamine; D017447:Receptors, Dopamine D1; D017448:Receptors, Dopamine D2; D015102:3,4-Dihydroxyphenylacetic Acid; D004054:Diethylstilbestrol; D011388:Prolactin; D000242:Cyclic AMP; D014446:Tyrosine 3-Monooxygenase; D004298:Dopamine