IQUIFIB   02644
INSTITUTO DE QUIMICA Y FISICOQUIMICA BIOLOGICAS "PROF. ALEJANDRO C. PALADINI"
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Prenatal stress effect on glutamatergic synthesis and uptake
Autor/es:
ADROVER E, KATUNAR M.R, PALLARES M.E, BAIER C.J, SCHOUSBOE A. Y ANTONELLI M.C
Reunión:
Congreso; V Congreso de la Sociedad de Neurotoxicidad (NTS); 2011
Resumen:
PRENATAL
STRESS EFFECT ON GLUTAMATERGIC SYNTHESIS AND UPTAKE.
Adrover E.1, Katunar
M.R.1, Pallares M.E.1, Baier C.J.1, Schousboe
A.2 y Antonelli M.C.1
1IQUIFIB
(UBA-CONICET), Facultad de Farmacia y Bioquímica. UBA. Buenos Aires. Argentina.
2Faculty of Pharmaceutical Sciences University of
Copenhagen. Copenhagen. Denmark.
Episodes of stress suffered by
the mother during pregnancy generate changes in the fetal environment affecting
central nervous system development of the offspring. Previous studies from our
laboratory have shown that adult offspring of stressed rats exhibited higher
levels of glutamate receptors than control rats. These animals also show long-lasting
astroglial reaction and a reduced dendritic arborization with synaptic loss.
Since metabolism of glutamate is linked to a cycle between neurons and
sorrounding astroglia, our results suggest that glutamate neurotransmitter
pathways might be impaired in the brain of a prenatally stressed rats. To study the
effect of prenatal stress (PS) on the metabolism of glutamate, pregnant rats
were subjected to restrain stress during the last week of gestation. Brain
extracts of PS rats were evaluated by mass spectroscopy to measure the content
of glutamate and other metabolites. The results show no differences between
control and PS animals in the glutamate metabolism. We also evaluated glutamate
uptake and the protein level of glutamate transporters. Our results show that
glutamate uptake of adult (PND 60) PS rats is significantly higher than in
control rats. This would indicate that prenatal stress produces long-term
changes in the glutamatergic system modulating the expression of glutamate
receptors and altering the normal synaptic transmission of the adult brain.