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DOPAMINERGIC NEUROTRANSMISSION IN A PRENATAL STRESS MODEL
KATUNAR MR1, ADROVER E1, BAIER CJ1, CALTANA L2 , PALLARÉS ME1, SAEZ T2, BRUSCO A2, AND ANTONELLI MC1
Congreso; V Congreso de la Sociedad de Neurotoxicidad (NTS); 2011
Rats exposed to different types of stress during the last week of pregnancy produce offspring that show severe anomalies in neural development and brain morphology that persist into adulthood particularly in dopaminergic neurotransmission. We have previously shown that prenatal stress (PS) increases dopamine (DA) D2-type receptor (D2R) levels in prefrontal cortex (PFc), nucleus accumbens (NAc) core and hippocampus (Hip) and a decrease of amphetamine stimulated DA levels in NAc shell and PFc. In this study we have demonstrated that PS produces changes in dopamine uptake in the adolescent and young adult offspring mainly in limbic areas whereas the dopaminergic metabolism is not affected. The expression of the enzyme tyrosine hidroxylase TH, was decreased at early developmental stages in the mesencephalic neuronal bodies whereas the activity was altered in limbic and motor areas at early adolescence. Dopamine related transcription factors Nurr1 and Pitx3 are highly vulnerable to PS and changes persist along development of the offsprings. Morphological studies revealed that PS offspring present a significant reduction in the dendritic arborization of mesencephalic structures suggesting that normal connectivity between areas might be impaired. Taking into consideration our results and those of the literature, we speculate that changes exerted on the dopaminergic limbic system by prenatal insults might be associate with behavioural disorders or neuropsychiatric pathologies with adolescent or young adult onset.