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表达NG2的神经胶质细胞的生理特征。

Physiological characteristics of NG2-expressing glial cells.

作者信息

Lin Shih-Chun, Bergles Dwight E

机构信息

Department of Neuroscience, Johns Hopkins University School of Medicine, 725 North Wolfe St., WBSB 813, Baltimore, MD 21205, USA.

出版信息

J Neurocytol. 2002 Jul-Aug;31(6-7):537-49. doi: 10.1023/a:1025799816285.

Abstract

Antibodies against the chondroitin sulfate proteoglycan NG2 label a subpopulation of glial cells within the CNS, which have a small cell body and thin radiating processes. Physiological recordings from these small cells in acute brain slices have revealed that they possess unique properties, suggesting that they may comprise a class of glial cells distinct from astrocytes, oligodendrocytes, or microglia. NG2-expressing glial cells (abbreviated as "NG2 cells" here) have a moderate input resistance and are not dye- or tracer-coupled to adjacent cells. They express voltage-gated Na+, K+ and Ca2+ conductances, though they do not exhibit regenerative Na+ or Ca2+ action potentials due to the much larger K+ conductances present. In addition to voltage-gated conductances, they express receptors for various neurotransmitters. In the hippocampus, AMPA and GABAA receptors on these cells are activated by release of transmitter from neurons at defined synaptic junctions that are formed with CA3 pyramidal neurons and GABAergic interneurons. These rapid forms of neuron-glial communication may regulate the proliferation rate of NG2 cells or their development into mature oligodendrocytes. These depolarizing inputs may also trigger the release of neuroactive substances from NG2 cells, providing feedback regulation of signaling at neuronal synapses. Although the presence of Ca2+ permeable AMPA receptors provides a pathway to link neuronal activity to Ca2+ dependent processes within the NG2 cells, these receptors also put these cells at risk for glutamate-associated excitotoxicity. This vulnerability to the sustained elevation of glutamate may underlie ischemic induced damage to white matter tracts and contribute to cerebral palsy in premature infants.

摘要

针对硫酸软骨素蛋白聚糖NG2的抗体可标记中枢神经系统内的一类神经胶质细胞亚群,这些细胞具有小的细胞体和细长的放射状突起。对急性脑片中小细胞的生理学记录显示,它们具有独特的特性,这表明它们可能构成一类与星形胶质细胞、少突胶质细胞或小胶质细胞不同的神经胶质细胞。表达NG2的神经胶质细胞(此处简称为“NG2细胞”)具有中等输入电阻,且不与相邻细胞进行染料或示踪剂偶联。它们表达电压门控的Na+、K+和Ca2+通道,尽管由于存在更大的K+通道,它们不会表现出再生性的Na+或Ca2+动作电位。除了电压门控通道外,它们还表达多种神经递质的受体。在海马体中,这些细胞上的AMPA和GABAA受体可被来自与CA3锥体神经元和GABA能中间神经元形成的特定突触连接处的神经元释放的递质激活。这些快速的神经元-神经胶质细胞通讯形式可能调节NG2细胞的增殖速率或其向成熟少突胶质细胞的发育。这些去极化输入也可能触发NG2细胞释放神经活性物质,从而对神经元突触处的信号传导提供反馈调节。尽管Ca2+通透的AMPA受体的存在提供了一条将神经元活动与NG2细胞内Ca2+依赖性过程联系起来的途径,但这些受体也使这些细胞面临与谷氨酸相关的兴奋性毒性风险。这种对谷氨酸持续升高的易感性可能是缺血诱导的白质损伤的基础,并导致早产儿的脑瘫。

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