IMBECU   20882
INSTITUTO DE MEDICINA Y BIOLOGIA EXPERIMENTAL DE CUYO
Unidad Ejecutora - UE
artículos
Título:
Role of Estradiol in the Regulation of Prolactin Secretion During Late Pregnancy.
Autor/es:
JAHN GA; VILLEGAS GABUTTI C; SOAJE M; PENNACCHIO GE
Revista:
NEUROCHEMICAL RESEARCH
Editorial:
SPRINGER/PLENUM PUBLISHERS
Referencias:
Lugar: New York; Año: 2016 vol. 41 p. 3344 - 3355
ISSN:
0364-3190
Resumen:
Abstract Estrogen action is necessary for evidencing thestimulatory action of mifepristone and naloxone on prolactin(PRL) secretion during late pregnancy. Our aim is todetermine the mechanism mediating this facilitator actionof estrogens. To investigate the hypothalamic mechanismsinvolved in estrogen actions in PRL secretion at the endof pregnancy, we measured the effect of pretreatment withthe estrogen antagonist tamoxifen on the expression oftyrosine hydroxylase (TH), hormone receptors (ERα andβ, PRs, PRLR(long)), and μ- and κ- opioid receptors (ORs)at mRNA (by semiquantitative RT-PCR) and protein (bywestern blot for TH, PRLR(long), ERα, PRs, μ- and ORs)levels in extracts of medial basal hypothalamus (MBH) andserum PRL, E2 and P4 levels (by RIA) in mifepristone- andnaloxone-treated rats. Tamoxifen administration partiallyprevented PRL release induced by the combined treatment.TH expression diminished and ERα expression increased inmifepristone-treated rats at mRNA and protein levels andtamoxifen partially prevented these changes with no effecton PRs expression. Mifepristone increased PRLR(long)mRNA levels; this increase was blocked by tamoxifen.Combined tamoxifen and mifepristone treatment decreasedμ- and k-ORs mRNA but not protein levels. In conclusion,E2 induces neuroadaptive mechanisms necessary to facilitatePRL release preceding delivery. Acting through ERα,E2 modulates hypothalamic dopaminergic neurons activity,regulating TH, μ- and κ-ORs and PRLR(long) expression,and is necessary for evidencing the effects of P4 withdrawal.Its presence on days 14 and 15 of pregnancy iscrucial to facilitate the opioid system modulation of PRLsecretion at the end of pregnancy in the rat.