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首页> 外文期刊>The European Journal of Neuroscience >Orexin (hypocretin) gene transfer diminishes narcoleptic sleep behavior in mice.
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Orexin (hypocretin) gene transfer diminishes narcoleptic sleep behavior in mice.

机译：食欲素（hypocretin）基因转移可减少小鼠的发作性睡眠行为。

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摘要

Gene transfer has proven to be an effective neurobiological tool in a number of neurodegenerative diseases, but it is not known if it can correct a sleep disorder. Narcolepsy is a neurodegenerative sleep disorder linked to the loss of neurons containing the neuropeptide orexin, also known as hypocretin. Here, a replication-defective herpes simplex virus-1 amplicon-based vector was constructed to transfer the gene for mouse prepro-orexin into mice with a genetic deletion of the orexin gene. After in vitro tests confirmed successful gene transfer into cells, the gene vector was delivered to the lateral hypothalamus of orexin knockout (KO) mice where the orexin peptide was robustly expressed in the somata and processes of numerous neurons, and the peptide product was detected in the cerebrospinal fluid. During the 4-day life-span of the vector the incidence of cataplexy declined by 60%, and the levels of rapid eye movement sleep during the second half of the night were similar to levels in wild-type mice,indicating that narcoleptic sleep-wake behavior in orexin KO mice can be improved by targeted gene transfer.
机译：基因转移已被证明是许多神经退行性疾病中有效的神经生物学工具，但尚不清楚它是否可以纠正睡眠障碍。发作性睡病是一种神经退行性睡眠障碍，与含有神经肽食欲素的神经元丢失有关，也被称为降血钙素。在这里，构建了基于复制缺陷的单纯疱疹病毒1扩增子的载体，以将用于小鼠前原胃泌素的基因转移到具有orexin基因的基因缺失的小鼠中。在体外测试证实基因成功转移到细胞中后，基因载体被递送到orexin敲除（KO）小鼠的下丘脑外侧，其中orexin肽在躯体和许多神经元的过程中强烈表达，并且在脑脊液。在载体的4天寿命中，白内障的发病率下降了60％，并且在下半夜的快速眼动睡眠水平与野生型小鼠的水平相似，这表明麻醉性睡眠- Orexin KO小鼠的唤醒行为可以通过靶向基因转移得到改善。

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