MILD HYPERTHYROIDISM AFFECTS PROLACTIN SECRETION INDUCED BY ACUTE STRESS IN LACTATING RATS

FLAVIA J. NEIRA; MARÍA B. SANCHEZ; MARÍA C. MICHEL; MARIANA TRONCOSO; ELISA O. PIETROBON; MARTA SOAJE; MACKERN-OBERTI JP; GRACIELA A. JAHN; SUSANA R. VALDEZ

Mendoza

Congreso; ‎XXXVII Reunión Científica Anual de la Sociedad de Biología de Cuyo; 2021

Hyperthyroidism (HyperT) has higher incidence in women than in men and can cause reproductive disorders affecting lactation. Pregnancy and lactation are regulated by intricate central neuroendocrine mechanisms present in areas such as the medial basal hypothalamus (MBH), the main neuronal group that regulates PRL secretion. PRL has various functions at the central level and its receptor is expressed in different brain regions that modulate the response to stress. We evaluated the effect of mild HyperT on PRL release in response to acute stress in lactating rats. HyperT was induced with T4 (0.1mg /kg/day, s.c.) a dose of that allows the maintenance of lactation. Control (Con) and HyperT female Wistar rats were bled from the tail vein during the 2 min ether exposure (s1) and 5 min after ether exposure (s2). We analyzed serum prolactin levels in day 19 of gestation (G19), 2 (L2) and 12 (L12) of lactation. To explore the neuroendocrine mechanisms of PRL release in lactation, we also determined by RT-qPCR the expression of thyroid receptor (TR), the long isoform of the prolactin receptor (PRLRl), members of the PRL signaling pathway (STAT5b; CIS; SOCS), progesterone receptor (PR), estrogen receptor (ER) and glucocorticoid receptor (GR) in MBH of rats in G19, L2 and L12 of lactation in non-stressed Con and HyperT groups. In G19 acute stress induced PRL release in HiperT (P