HIPPOCAMPAL HORMONE RECEPTORS EXPRESSION IN LATE PREGNANT AND LACTATING RATS: EFFECT OF MILD HYPERTHYROIDISM

FLAVIA J. NEIRA; MARÍA B. SANCHEZ; ELISA O. PIETROBON; J.P. MACKERN-OBERTI; MARTA SOAJE; GRACIELA A. JAHN; SUSANA R. VALDEZ

Buenos Aires

Congreso; Reunión Anual de SOCIEDADES DE BIOCIENCIAS. SAIC. SAFE. SAB. SAP. AACYTAL. NANOMED.; 2019

Thyroid disorders are associated with anxiety, depression and disturb responses to stress. The effect of stress is associated with functional changes in hippocampus (HpC) and hypothalamus by activating the hypothalamichypophysis-adrenal axis (HHA) and glucocorticoid release induced to stress. This response is physiologically attenuated during lactation. We found that mild hyperthyroidism (HyperT) increases stress-induced serum prolactin (PRL) and corticosterone secretion in lactating rats suggesting that HHA remains activated in lactation. To explore possible causes of this effect we studied the expression of thyroid receptors (TR), the long isoform of PRL receptor (PRLRl), members of the PRL signaling pathway, estradiol receptor (ER) and glucocorticoid receptor (GR) in HpC of Wistar female rats in different reproductive states (day 19 of gestation (G19), 2 (L2, early lactation) and 12 (L12) of lactation) in control (Co) and HyperT rats. Mild HyperT was induced with T4 (0.1 mg/kg/day, s.c.), a dose that allows the maintenance of lactation. HpC mRNA was obtained and the expression of receptors TRa1, TRa2, TRb1, TRb2, ERa, GR and PRLRl and members of the PRL signaling pathway (STAT5b, SOCS1 and SOCS3) was determined by RTqPCR. HpC mRNA content of TRs, STAT5b (activator of PRL signaling) and SOCS1 (supressor of PRL signaling) decreased from G19 to L12 in Co and HyperT rats (p