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Calcium Signaling in the Oligodendrocyte Lineage: Regulators and Consequences.
Annual Review of Neuroscience ( IF 13.9 ) Pub Date : 2020-07-08 , DOI: 10.1146/annurev-neuro-100719-093305
Pablo M Paez 1 , David A Lyons 2
Affiliation  

Cells of the oligodendrocyte lineage express a wide range of Ca2+ channels and receptors that regulate oligodendrocyte progenitor cell (OPC) and oligodendrocyte formation and function. Here we define those key channels and receptors that regulate Ca2+ signaling and OPC development and myelination. We then discuss how the regulation of intracellular Ca2+ in turn affects OPC and oligodendrocyte biology in the healthy nervous system and under pathological conditions. Activation of Ca2+ channels and receptors in OPCs and oligodendrocytes by neurotransmitters converges on regulating intracellular Ca2+, making Ca2+ signaling a central candidate mediator of activity-driven myelination. Indeed, recent evidence indicates that localized changes in Ca2+ in oligodendrocytes can regulate the formation and remodeling of myelin sheaths and perhaps additional functions of oligodendrocytes and OPCs. Thus, decoding how OPCs and myelinating oligodendrocytes integrate and process Ca2+ signals will be important to fully understand central nervous system formation, health, and function.

中文翻译:


少突胶质细胞谱系中的钙信号传导:调节剂和后果。

少突胶质细胞谱系的细胞表达多种 Ca 2+通道和受体,可调节少突胶质祖细胞 (OPC) 和少突胶质细胞的形成和功能。在这里,我们定义了那些调节 Ca 2+信号传导和 OPC 发育和髓鞘形成的关键通道和受体。然后我们讨论细胞内 Ca 2+的调节如何反过来影响健康神经系统和病理条件下的 OPC 和少突胶质细胞生物学。神经递质对 OPCs 和少突胶质细胞中 Ca 2+通道和受体的激活集中于调节细胞内 Ca 2+,使 Ca 2+向活动驱动的髓鞘形成的中心候选介质发出信号。事实上,最近的证据表明少突胶质细胞中 Ca 2+ 的局部变化可以调节髓鞘的形成和重塑,并且可能调节少突胶质细胞和 OPCs 的其他功能。因此,解码 OPCs 和髓鞘化少突胶质细胞如何整合和处理 Ca 2+信号对于充分了解中枢神经系统的形成、健康和功能非常重要。

更新日期:2020-07-09
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