Ochi Shinichiro, Abe Masao, Li Cheng, Mori Yoko, Ishimaru Takashi, Yoshino Yuta, Yamazaki Kiyohiro, Mori Takaaki, Fukuhara Ryuji, Tanimukai Satoshi, Matsuda Seiji, Yoshida Kenichi, Ueno Shu-ichi
Department of Neuropsychiatry, Ehime University Graduate School of Medicine, Toon 791-0295, Ehime, Japan.
Department of Neuropsychiatry, Ehime University Graduate School of Medicine, Toon 791-0295, Ehime, Japan.
Neurosci Lett. 2014 May 21;569:33-7. doi: 10.1016/j.neulet.2014.03.054. Epub 2014 Apr 2.
Delayed carbon monoxide (CO) encephalopathy may occur following recovery from acute CO poisoning. However, the mechanism of delayed neuronal injury remains unknown. The nicotinic acetylcholine receptors (nAChRs) have been suggested to play a role in cognitive status in neurodegenerative diseases, including Alzheimer's disease. Therefore, in the current study, we investigated the effect of delayed neuronal CO poisoning on gene expression of nAChRs in the hippocampus of Wistar rats. Behavioral effects (measured by the passive-avoidance test) and histological analyses (hematoxylin-eosin-stained hippocampal cell counts and cell death observations) were also investigated, 21 days after CO exposure for 1h (1000ppm for 40min+3000ppm for 20min). Our findings show cognitive impairment and hippocampal cell death, suggesting our rat model is suitable for studying delayed CO encephalopathy. Expression of nAChR (Chrna3, Chrna4, Chnra7, and Chrnb2) mRNA was assessed using quantitative real-time polymerase chain reaction. Hippocampal Chrna3 expression was significantly decreased, and cerebellar Chrna7 expression significantly increased, in the delayed CO encephalopathy rat model. Thus, the nicotinic cholinergic system may be affected in delayed CO encephalopathy.
急性一氧化碳（CO）中毒恢复后可能会发生迟发性一氧化碳脑病。然而，迟发性神经元损伤的机制尚不清楚。烟碱型乙酰胆碱受体（nAChRs）已被认为在包括阿尔茨海默病在内的神经退行性疾病的认知状态中起作用。因此，在本研究中，我们调查了迟发性神经元CO中毒对Wistar大鼠海马中nAChRs基因表达的影响。在CO暴露1小时（1000ppm持续40分钟 + 3000ppm持续20分钟）后21天，还研究了行为效应（通过被动回避试验测量）和组织学分析（苏木精 - 伊红染色的海马细胞计数和细胞死亡观察）。我们的研究结果显示出认知障碍和海马细胞死亡，表明我们的大鼠模型适用于研究迟发性CO脑病。使用定量实时聚合酶链反应评估nAChR（Chrna3、Chrna4、Chnra7和Chrnb2）mRNA的表达。在迟发性CO脑病大鼠模型中，海马Chrna3表达显著降低，小脑Chrna7表达显著增加。因此，烟碱胆碱能系统可能在迟发性CO脑病中受到影响。
