Prenatal Restraint Stress and Vulnerability of Dopaminergic Neurons

BAIER CJ; KATUNAR MR; ADROVER E; PALLARÉS ME; RAISMAN-VOZARI R; ANTONELLI MC

Uspallata, Mendoza

Congreso; V Neurotoxicity Society Meeting; 2011

NTS

It has been demonstrated in animal models that maternal disturbance can influence the offspring’s brain chemistry, endocrine function, emotionality, and learning ability. Exposure to adverse events in early life can alter adult behaviors and neurochemical indicators of midbrain dopamine (DA) activity, suggesting that the development of the DA system is sensitive to disruption by brief exposure to early stressors. In humans, dysfunction of dopaminergic system is associated with development of several neurological disorders such as Parkinson’s disease (PD), schizophrenia, attention-deficit hyperactivity disorder and depression. The pathological hallmark of PD is the relatively selective loss of DA neurons in the substantia nigra compacta (SNc) in the ventral midbrain with posterior loss of DA in the nigroestriatal system, and presence of cell bodies enriched in -synuclein aggregates. Oxidative stress and neuroinflammation participate in the pathogenesis of PD. The neurotoxin 6-hydroxydopamine (6-OHDA) is a classical and valuable model of PD in the rat. The aim of the present study was to investigate whether prenatal restrain stress increases the vulnerability of DA neurons to degenerate after striatal 6-OHDA injection in the adulthood. Dopaminergic neuron degeneration was determined by tirosine hydroxylase (TH) immunohistochemistry in striatum and SNc. We found no significant differences in TH levels between control and prenatally stressed animals treated with 6-OHDA in both areas. Additionally we investigated the expression and localization of neuronal nitric oxide synthase and glial markers in prenatally stressed rats. This study was supported in part by FONCYT and Bernardo Houssay Program