EFFECT OF MILD HYPERTHYROIDISM ON GLUCOCORTICOID SECRETION INDUCED BY ACUTE STRESS IN PREGNANCY AND LACTATING RATS

NEIRA FLAVIA J; MORENO SOSA MARÍA TAMARA; VALDEZ SUSANA RUTH; SANCHEZ MARÍA BELÉN; JAHN GRACIELA A; PIETROBON ELISA O; SOAJE, MARTA

Mendoza

Congreso; XXXVI Reunión Anual de la Sociedad de Biología de Cuyo; 2019

Sociedad de Biología de Cuyo

Disorders in thyroid functionare associated with anxiety and depression. Therefore, responses to stress maybe altered in patients with thyroid diseases. Stress is associated withfunctional changes in brain areas such as the hippocampus (HpC) and medialbasal hypothalamus (MBH) by activating the hypothalamic-hypophysis-adrenal axis(H-H-A) and the consequent release of glucocorticoids in response to thestressor. In this study we analyzed the effects of mild hyperthyroidism oncorticosterone response (measured by RIA) to acute stress (exposure to ethervapors for 2 min.) and on the expression (by qPCR) of the glucocorticoidreceptor (GR) and the long isoform of the prolactin receptor (PRLRL) in MBH and HpCin Wistar female rats in different reproductive states (day 19 of gestation(G19), 2 (L2) and 12 (L12) of lactation). Hyperthyroidism (hyperT) was inducedwith T4 (0.1mg /kg/day, s.c.) a dose of that allows the maintenance oflactation. Control (Co) and hyperT rats were bled from the tail vein during the2 min ether exposure (s1) and 5 min after ether exposure (s2). In G19 acutestress induced corticosterone release in Co group (P