| Parkinson's disease (PD) is an age-related neurodegenerative disosder characterized by selective loss of dopaminergic (DA) neurons in the substantia nigra (SN). Although a genetic basis accounts for some cases, the majority of PD is idiopathic. Environmental toxins have been proposed to contribute to the pathogenesis of PD. To date, all studies evaluating the role of environmental neurotoxins in PD have assumed exposure during adult life, but our recent data suggests a potential role for prenatal neurotoxin exposure as well. We have demonstrated that injection of endotoxin lipopolysaccharide (LPS) into gravid female at embryonic day 10.5 (E10.5) resulted in the birth of animals with fewer DA neurons at postnatal days 21(P21). The reduction in DA neurons is associated with reductions in striatal DA and increased DA activity in the striatum. These suggest that LPS may be a potential toxin to replicate DA neurons loss model. However, the mechanism responsible for LPS-induced DA neurons loss is currently unknown.Bacterial vaginosis (BV) commonly occurs in pregnancy and is widely believed to lead to serious perinatal complications. BV often does not produce signs of overt infection aside from a vaginal discharge and, as a result, generally goes untreated. Increasing evidences reveal that BV is clearly associated with increased levels of LPS, interleukin 1β(IL-1β), tumor necrosis factorα(TNF-α) in the chorioamniotic environment. BV is presumed to be the leading cause of premature deliverl and low birth weigh. It is also feasible that maternal LPS will trigger cytokine production by fetal tissues which then mediate LPS-induced DA cell loss. In deed, BV has been linked to numerous neurological disorders including white matter damage and cerebral palsy. Taken together, prenatal infection such as BV could lead to abnormal environment for development of DA system.Thus, this study intends to test the overall hypothesis that prenatal exposure to LPS leads...
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