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

Laboratory Animal Research volume 33, pages 244–250 (2017)Cite this article

Abstract

α-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 α-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 α-synuclein in the cerebral cortices after MCAO injury. Moreover, glutamate treatment induced neuronal cell death and decreased α-synuclein expression in a hippocampal-derived cell line in a dose-dependent manner. It is known that α-synuclein regulates neuronal survival, and low levels of α-synuclein expression result in cytotoxicity. Thus, these results suggest that cerebral ischemic injury leads to a reduction in α-synuclein and consequently causes serious brain damage.

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Authors and Affiliations

  1. Department of Anatomy, College of Veterinary Medicine, Gyeongsang National University, 501 Jinjudaero, Jinju, 52828, Korea

    Phil-Ok Koh

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  1. Phil-Ok Koh
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Koh, PO. Cerebral ischemic injury decreases α-synuclein expression in brain tissue and glutamate-exposed HT22 cells. Lab Anim Res 33, 244–250 (2017). https://doi.org/10.5625/lar.2017.33.3.244

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  • DOI: https://doi.org/10.5625/lar.2017.33.3.244

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Laboratory Animal Research

ISSN: 2233-7660