IQUIFIB   02644
INSTITUTO DE QUIMICA Y FISICOQUIMICA BIOLOGICAS "PROF. ALEJANDRO C. PALADINI"
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
“Prenatal stress effects on morphological and neuroendocrine aspects of male rats progeny”
Autor/es:
PALLARÉS M.E; GONZÁLEZ-CALVAR S.I; BOURGUIGNON N.S; ADROVER E; KATUNAR M.R.; BAIER C.J.; LUX-LANTOS V; CALANDRA R.S; ANTONELLI M.C
Lugar:
Valdivia
Reunión:
Congreso; VI reunion anual de la Sociedad Chilena de Neurociencias; 2010
Institución organizadora:
Sociedad Chilena de Neurociencias (SCN)
Resumen:
We have previously demonstrated that prenatal stress (PS) exerted an impairment of dopaminergic (DA) metabolism in limbic brain areas especially after puberty. In this study we evaluated hypothalamic- pituitary- testicular (HPT) axis status of males exposed to PS. Stress consisted on a 3 daily- 45min restraint session from day 14th of gestation to delivery. Anogenital distances and testis descent were measured at postnatal day (PND) 21. Luteinizing hormone (LH), Testosterone (T) and 5-a Androstane- 3-a, 17b- Diol (DIOL) serum levels of 28, 35, 45, 60 and 75 days old male progeny were determined by radioimmunoassay. Testes of 35 and 60 days old animals were processed for histological morphometric measures. PS reduced anogenital distance of PND 21 male offspring and induced a 2-day delay in the completion of testis descent, in comparison to controls (C). Hormones serum levels analyses revealed that PS diminished LH at PND 28 and 75 (88 and 65,6%), decreased T serum levels at 75 days old rats (58,6%), and increased DIOL levels at PND 28 and 45 (61 and 63%). Additionally, the rate of spermatogenesis development was accelerated on PS rats and the mean tubular diameter was increased. However, the mean Leydig cell’s number was reduced on PS rats. Our results demonstrate that stress during gestation induces long term effects on the male progeny HPT axis. Since it was reported that gonadal hormones produce plastic changes in the brain, a disbalanced hormone milieu might be responsible of the DA metabolism impairment observed in our previous studies.