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Gabapentin receptor alpha2delta-1 is a neuronal thrombospondin receptor responsible for excitatory CNS synaptogenesis.加巴喷丁受体α2δ-1是一种神经元凝血酶敏感蛋白受体,负责中枢神经系统兴奋性突触的形成。
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Regulated release of BDNF by cortical oligodendrocytes is mediated through metabotropic glutamate receptors and the PLC pathway.皮质少突胶质细胞通过代谢型谷氨酸受体和 PLC 途径调节 BDNF 的释放。
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Rett syndrome astrocytes are abnormal and spread MeCP2 deficiency through gap junctions.雷特综合征星形胶质细胞异常,并通过缝隙连接传播MeCP2缺乏症。
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In situ hybridization reveals developmental regulation of ErbB1-4 mRNA expression in mouse midbrain: implication of ErbB receptors for dopaminergic neurons.原位杂交揭示小鼠中脑中ErbB1 - 4 mRNA表达的发育调控:ErbB受体对多巴胺能神经元的影响。
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The mystery and magic of glia: a perspective on their roles in health and disease.神经胶质细胞的奥秘与魔力:关于它们在健康与疾病中作用的观点
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Reciprocal regulation of presynaptic and postsynaptic proteins in bipolar spiral ganglion neurons by neurotrophins.神经营养因子对双极螺旋神经节神经元突触前和突触后蛋白的相互调节
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10
Type III neuregulin-1 promotes oligodendrocyte myelination.III型神经调节蛋白-1促进少突胶质细胞髓鞘形成。
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非神经元细胞通过 erbB 依赖性 BDNF 表达调控前庭感觉上皮中的突触形成。

Nonneuronal cells regulate synapse formation in the vestibular sensory epithelium via erbB-dependent BDNF expression.

机构信息

F. M. Kirby Neurobiology Center, Children's Hospital Boston, Boston, MA 02115, USA.

出版信息

Proc Natl Acad Sci U S A. 2010 Sep 28;107(39):17005-10. doi: 10.1073/pnas.1008938107. Epub 2010 Sep 13.

DOI:10.1073/pnas.1008938107
PMID:20837532
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2947909/
Abstract

Recent studies indicate that molecules released by glia can induce synapse formation. However, what induces glia to produce such signals, their identity, and their in vivo relevance remain poorly understood. Here we demonstrate that supporting cells of the vestibular organ--cells that have many characteristics of glia--promote synapse formation only when induced by neuron-derived signals. Furthermore, we identify BDNF as the synaptogenic signal produced by these nonneuronal cells. Mice in which erbB signaling has been eliminated in supporting cells have vestibular dysfunction caused by failure of synapse formation between hair cells and sensory neurons. This phenotype correlates with reduced BDNF expression in supporting cells and is rescued by reexpression of BDNF in these cells. Furthermore, knockdown of BDNF expression in supporting cells postnatally phenocopies the loss of erbB signaling. These results indicate that vestibular supporting cells contribute in vivo to vestibular synapse formation and that this is mediated by reciprocal signals between sensory neurons and supporting cells involving erbB receptors and BDNF.

摘要

最近的研究表明,神经胶质细胞释放的分子可以诱导突触形成。然而,是什么诱导神经胶质细胞产生这种信号,它们的身份以及它们在体内的相关性仍知之甚少。在这里,我们证明前庭器官的支持细胞——具有许多神经胶质细胞特征的细胞——只有在受到神经元衍生信号诱导时才促进突触形成。此外,我们确定 BDNF 是这些非神经元细胞产生的促突触形成信号。在支持细胞中消除 erbB 信号的小鼠由于毛细胞和感觉神经元之间的突触形成失败而出现前庭功能障碍。这种表型与支持细胞中 BDNF 表达减少相关,并且可以通过在这些细胞中重新表达 BDNF 来挽救。此外,支持细胞中 BDNF 表达的敲低在出生后模拟了 erbB 信号的缺失。这些结果表明,前庭支持细胞在体内有助于前庭突触的形成,并且这是由涉及 erbB 受体和 BDNF 的感觉神经元和支持细胞之间的相互信号介导的。