The regulation of GnRH by prolactin is associated to corpora lutea activity during pregnancy in the south American plains vizcacha, Lagostomus maximus.

CORTASA SA; CORSO MC; VITULLO AD; SCHMIDT AR; INSERRA PIF; HALPERÍN J; DORFMAN VB; PROIETTO S; DI GIORGIO NP

Concón

Congreso; 29ª Reunión Anual de la Sociedad Chilena de Reproducción y Desarrollo; 2018

Prolactin (PRL) promotes luteal steroidogenesis in rodents and inhibits hypothalamic?hypophyseal?ovaric axis during pregnancy. The South American plains vizcacha shows GnRH increase at mid-pregnancy with ovulation and corpora lutea (CL) formation. Herein, we investigated PRL modulation of GnRH expression and delivery and its relation to the CL development during gestation. We designed 2 experiments: 1) study of total release of GnRH from hypothalamic explants (eHT) of non-pregnant vizcachas cultured for 6hs in media supplemented with either hyperprolactinemic or control serum (n=5), 2) analysis of GnRH pulsatility in eHT of females treated for 7 days with Sulpiride (20mg/Kg,n=5) or with saline solution (controls). In addition, hypothalamic immunoexpression of GnRH, dopamine receptor (DR2), tyrosin hydroxylase (TH) and PRL receptor (PRLR) was studied in early-, mid- and term-gestating vizcachas (n=5/group). The mass of GnRH released from eHT incubated for 6hs with hyperprolactinemic serum was significantly increased related to controls (p<0.05). However, GnRH pulsatility was lower in hyperprolactinemic eHT compared to controls (p<0.05). The expression of GnRH, TH, DR2 and PRLR was studied in the hypothalamus of pregnant vizcachas to associate it with the dual effect of PRL on GnRH. TH-immunoreactive neurons were localized in the neighboring of GnRH-cells, whereas co-localization of GnRH with DR2, and of TH with PRLR, progressively increased during pregnancy. These results suggest that the increase of GnRH at mid-gestation is induced by the concomitant increase of PRL which is also involved in CL formation, whereas the sustained exposition to PRL up to the term-gestation inhibits GnRH pulsatility. Funding: Fundación Científica Felipe Fiorellino, PIP110/14, PICT1281/2014.