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少突胶质细胞生理学。

Physiology of Oligodendroglia.

机构信息

School of Pharmacy and Biomedical Science, University of Portsmouth, St Michael's Building, White Sawn Road, Portsmouth, PO1 2DT, UK.

出版信息

Adv Exp Med Biol. 2019;1175:117-128. doi: 10.1007/978-981-13-9913-8_5.

Abstract

Oligodendrocytes are the myelinating cells of the CNS, producing the insulating myelin sheath that facilitates rapid electrical conduction of axonal action potentials. Oligodendrocytes arise from oligodendrocyte progenitor cells (OPCs) under the control of multiple factors, including neurotransmitters and other neuron-derived factors. A significant population of OPCs persists in the adult CNS, where they are often referred to as NG2-glia, because they are identified by their expression of the NG2 chondroitin sulphate proteoglycan (CSPG4). In the adult brain, the primary function of NG2-glia is the life-long generation of oligodendrocytes to replace myelin lost through natural 'wear and tear' and pathology, as well as to provide new oligodendrocytes to myelinate new connections formed in response to new life experiences. NG2-glia contact synapses and respond to neurotransmitters and potassium released during neuronal transmission; to this end, NG2-glia (OPCs) express multiple neurotransmitter receptors and ion channels, with prominent roles being identified for glutamatergic signalling and potassium channels in oligodendrocyte differentiation. Myelinating oligodendrocytes also express a wide range of neurotransmitter receptors and ion channels, together with transporters and gap junctions; together, these have critical functions in cellular ion and water homeostasis, as well as metabolism, which is essential for maintaining myelin and axon integrity. An overriding theme is that oligodendrocyte function and myelination is not only essential for rapid axonal conduction, but is essential for learning and the long-term integrity of axons and neurones. Hence, myelination underpins cognitive function and the massive computing power of the human brain and myelin loss has devastating effects on CNS function. This chapter focuses on normal oligodendrocyte physiology.

摘要

少突胶质细胞是中枢神经系统的髓鞘形成细胞,产生绝缘髓鞘,促进轴突动作电位的快速电传导。少突胶质细胞由少突胶质前体细胞(OPC)产生,受多种因素的控制,包括神经递质和其他神经元衍生因子。在成人中枢神经系统中存在大量的 OPC,它们通常被称为 NG2-胶质细胞,因为它们表达 NG2 软骨素硫酸蛋白聚糖(CSPG4)。在成人脑中,NG2-胶质细胞的主要功能是终生产生少突胶质细胞,以替代因自然“磨损”和病理学而丢失的髓鞘,并为响应新的生活经历而形成的新连接提供新的少突胶质细胞来髓鞘化。NG2-胶质细胞与突触接触,并对神经元传递过程中释放的神经递质和钾作出反应;为此,NG2-胶质细胞(OPC)表达多种神经递质受体和离子通道,其中谷氨酸能信号和钾通道在少突胶质细胞分化中的作用得到了明确的鉴定。髓鞘形成的少突胶质细胞还表达广泛的神经递质受体和离子通道,以及转运体和缝隙连接;这些共同在细胞离子和水稳态以及代谢中发挥关键作用,这对于维持髓鞘和轴突的完整性至关重要。一个主要的主题是,少突胶质细胞的功能和髓鞘形成不仅对快速轴突传导至关重要,而且对学习和轴突和神经元的长期完整性至关重要。因此,髓鞘形成是认知功能和人类大脑巨大计算能力的基础,髓鞘丢失对中枢神经系统功能有毁灭性的影响。本章重点介绍正常的少突胶质细胞生理学。

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