Cerebral ischemic injury decreases α-synuclein expression in brain tissue and glutamate-exposed HT22 cells

${\alpha}$-Synuclein is abundantly expressed in neuronal tissue, plays an essential role in the pathogenesis of neurodegenerative disorders, and exerts a neuroprotective effect against oxidative stress. Cerebral ischemia causes severe neurological disorders and neuronal dysfunction. In this study, we examined ${\alpha}$-synuclein expression in middle cerebral artery occlusion (MCAO)-induced cerebral ischemic injury and neuronal cells damaged by glutamate treatment. MCAO surgical operation was performed on male Sprague-Dawley rats, and brain samples were isolated 24 hours after MCAO. We confirmed neurological behavior deficit, infarction area, and histopathological changes following MCAO injury. A proteomic approach and Western blot analysis demonstrated a decrease in ${\alpha}$-synuclein in the cerebral cortices after MCAO injury. Moreover, glutamate treatment induced neuronal cell death and decreased ${\alpha}$-synuclein expression in a hippocampal-derived cell line in a dose-dependent manner. It is known that ${\alpha}$-synuclein regulates neuronal survival, and low levels of ${\alpha}$-synuclein expression result in cytotoxicity. Thus, these results suggest that cerebral ischemic injury leads to a reduction in ${\alpha}$-synuclein and consequently causes serious brain damage.