The pathogenesis study in rats with delayed carbon monoxide encephalopathy

Research Project

Project/Area Number	16K21207
Research Category	Grant-in-Aid for Young Scientists (B)
Allocation Type	Multi-year Fund
Research Field	Psychiatric science Emergency medicine
Research Institution	Ehime University
Principal Investigator	Ochi Shinichiro 愛媛大学, 医学系研究科, 助教 (40568911)
Research Collaborator	Ueno Shuichi 愛媛大学, 大学院医学系研究科, 教授 (80232768) Iga Jun-ichi 愛媛大学, 大学院医学系研究科, 准教授 (70363140) Nishihara Tasuku 愛媛大学, 医学部附属病院, 助教 (50568912)
Project Period (FY)	2016-04-01 – 2018-03-31
Project Status	Completed (Fiscal Year 2017)
Budget Amount *help	¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000) Fiscal Year 2017: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000) Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Keywords	間歇型一酸化炭素中毒 / ミクログリア / アストロサイト / 神経幹細胞 / マイクログリア / 海馬神経細胞新生 / 認知機能低下 / 脳・神経 / 遺伝子 / 細胞・組織 / 免疫学
Outline of Final Research Achievements	Rats were exposed to carbon monoxide (CO) until they lost consciousness. Behavioral effects on learning and memory function were measured by the passive-avoidance test until 3 weeks. The latencies were significantly shorter in the CO models. Immunohistochemical analyses revealed cell numbers in SOX2 positive cells and microglia tended to decrease CO models less than controls in the dentate gyrus. Especially, a lot of morphologically abnormal microglia was found. On the other hand, astrocytes tends to increase CO models more than controls in the dentate gyrus. Flow cytometry analyses revealed that the cell numbers of microglia were significantly reduced in CO models. These results suggested that delayed CO encephalopathy may occur the abnormalities in glial cells such as microglia and astrocytes, and reduce neural precursor cells. Thus, the impairment of neural precursor cells via abnormalities of glial cells may be affected in the mechanism of delayed neuronal injury.