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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Loss of erbB signaling in oligodendrocytes alters myelin and dopaminergic function, a potential mechanism for neuropsychiatric disorders
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Loss of erbB signaling in oligodendrocytes alters myelin and dopaminergic function, a potential mechanism for neuropsychiatric disorders

机译：少突胶质细胞中erbB信号的丢失改变了髓鞘和多巴胺能功能，这是神经精神疾病的潜在机制

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摘要

Several psychiatric disorders are associated with white matter defects, suggesting that oligodendrocyte (OL) abnormalities underlie some aspects of these diseases. Neuregulin 1 (NRG1) and its receptor, erbB4, are genetically linked with susceptibility to schizophrenia and bipolar disorder. In vitro studies suggest that NRG1-erbB signaling is important for OL development. To test whether erbB signaling contributes to psychiatric disorders by regulating the structure or function of OLs, we analyzed transgenic mice in which erbB signaling is blocked in OLs in vivo. Here we show that loss of erbB signaling leads to changes in OL number and morphology, reduced myelin thickness, and slower conduction velocity in CNS axons. Furthermore, these transgenic mice have increased levels of dopamine receptors and transporters and behavioral alterations consistent with neuropsychiatric disorders. These results indicate that defects in white matter can cause alterations in dopaminergic function and behavior relevant to neuropsychiatric disorders.
机译：几种精神疾病与白质缺陷有关，表明少突胶质细胞（OL）异常是这些疾病的某些方面。神经调节蛋白1（NRG1）及其受体erbB4与精神分裂症和双相情感障碍的易感性遗传相关。体外研究表明，NRG1-erbB信号传导对于OL的发展很重要。为了测试erbB信号是否通过调节OL的结构或功能来促进精神疾病，我们分析了erbB信号在OL中体内被阻断的转基因小鼠。在这里，我们表明erbB信号的丢失导致OL数量和形态的变化，髓鞘厚度的减少以及中枢神经系统轴突传导速度的降低。此外，这些转基因小鼠的多巴胺受体和转运蛋白水平增加，并且行为改变与神经精神疾病一致。这些结果表明，白质中的缺陷可引起多巴胺能功能和与神经精神疾病有关的行为的改变。

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