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Title: Effect of Dietary Selenium Exposure in the Striatal 6-OHDA Model of Parkinson's Disease
Student: Kanizeh Visram
Faculty advisor: Dr. Cecilia Fox
Parkinson's disease is a debilitating neurodegenerative disorder resulting from the gradual deterioration of the nigrostriatal pathway. A large body of research implicates free-radical oxidative damage as a potential mechanism for this neuronal loss. Therefore, it is reasonable to propose that antioxidant therapy may be neuroprotective, and slow the progression of the disease. The antioxidant, selenium is an essential element in the diet of all mammals. It resides in the active center of the free-radical-scavenging enzyme, glutathione peroxidase, which assists in the protection of membrane lipids and molecules from oxidative damage. This study was designed to test the efficacy of long-term dietary selenium administration on the rotation behavior in rodents challenged by a 6-hydroxydopamine (6-OHDA) striatal lesion. Fisher 344 rats were divided into two groups: control chow and chow supplemented with selenium (2ppm). Baseline rotation behavior testing was performed on both groups for two weeks using either 0.1mg/kg apomorphine (subcutaneous injection), or 5 mg/kg amphetamine (intraperitoneal injection). Following baseline testing, rats were treated with an intrastriatal 6-OHDA lesion. Apomorphine and amphetamine rotation behavior testing was performed for eight weeks post-lesion before all rats were euthanized by intracardiac perfusion. Brain tissue was processed for tyrosine hydroxylase immunocytochemical staining and cell survival analysis.