CONICET | Buscador de Institutos y Recursos Humanos

It is well known that animals exposed to stressful stimuli during their early life develop different neurological disorders when they become adults. In this study, we evaluated the consequences of acute and chronic stress on adult brain on Glutamate transporter (GluT) in vitro, evaluating the uptake of [3H]Glu by synaptosomes-enriched fractions isolated from rat cerebral frontal cortex (FC) and hippocampus (HIC) by time-course and kinetic studies. In acute stress, the rats were separated from their mothers at postnatal day (PD) 7 and divided in two groups: control and stress. While control rats were moved to a separated cage, stress rats were exposed to cold stress (4ºC) during 1 h. In repeated stress the rats were separated from their mothers and exposed to cold stress (4ºC) for 1 h at postnatal day (PD) 7 during 20 days. These animals were allowed to a 30 days recovery period until adulthood. At the end of the stress period, animals were killed by decapitation. FC and HIC were dissected to study GluT and trunk blood samples were collected to determinate corticosterone levels. Acute stress results show an HIC increase in both affinity and maximum velocity (Vmax), while in the FC only the affinity was increased. Repeated chronic stress shows changes only in Vmax: rise in FC and decrease in HIC. The time-course test on FC in acute stress shows an uptake decrease while in chronic stress the uptake was similar in both groups. HIC did not show significant differences either chronic or acute stress. The levels of corticosterone decrease either acute or chronic stress. These results suggest that the exposure to early stressful adverse life events affects hypothalamic-pituitary-adrenal (HPA) axis and alter the glutamatergic neurons.

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