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γ-氨基丁酸能信号在髓鞘可塑性与修复中的治疗潜力

Therapeutic Potential of GABAergic Signaling in Myelin Plasticity and Repair.

作者信息

Reyes-Haro Daniel, Cisneros-Mejorado Abraham, Arellano Rogelio O

机构信息

Instituto de Neurobiología, Universidad Nacional Autónoma de México Campus Juriquilla, Juriquilla, Mexico.

出版信息

Front Cell Dev Biol. 2021 Apr 6;9:662191. doi: 10.3389/fcell.2021.662191. eCollection 2021.

DOI:10.3389/fcell.2021.662191
PMID:33889577
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8056019/
Abstract

Oligodendrocytes (OLs) produce myelin to insulate axons. This accelerates action potential propagation, allowing nerve impulse information to synchronize within complex neuronal ensembles and promoting brain connectivity. Brain plasticity includes myelination, a process that starts early after birth and continues throughout life. Myelin repair, followed by injury or disease, requires new OLs differentiated from a population derived from oligodendrocyte precursor cells (OPCs) that continue to proliferate, migrate and differentiate to preserve and remodel myelin in the adult central nervous system. OPCs represent the largest proliferative neural cell population outside the adult neurogenic niches in the brain. OPCs receive synaptic inputs from glutamatergic and GABAergic neurons throughout neurodevelopment, a unique feature among glial cells. Neuron-glia communication through GABA signaling in OPCs has been shown to play a role in myelin plasticity and repair. In this review we will focus on the molecular and functional properties of GABA receptors (GABA Rs) expressed by OPCs and their potential role in remyelination.

摘要

少突胶质细胞(OLs)产生髓磷脂以包裹轴突。这加速了动作电位的传播,使神经冲动信息能够在复杂的神经元集合中同步,并促进大脑的连通性。脑可塑性包括髓鞘形成,这一过程在出生后早期开始并持续终生。在损伤或疾病后,髓鞘修复需要新的少突胶质细胞,这些细胞由少突胶质前体细胞(OPCs)分化而来,OPCs会持续增殖、迁移和分化,以在成体中枢神经系统中维持和重塑髓鞘。OPCs是大脑成体神经发生微环境之外最大的增殖性神经细胞群体。在整个神经发育过程中,OPCs接收来自谷氨酸能和γ-氨基丁酸能神经元的突触输入,这是胶质细胞中的一个独特特征。已证明通过OPCs中的γ-氨基丁酸信号进行的神经元-胶质细胞通讯在髓鞘可塑性和修复中起作用。在本综述中,我们将重点关注OPCs表达的γ-氨基丁酸受体(GABA Rs)的分子和功能特性及其在髓鞘再生中的潜在作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/535d/8056019/acadee797383/fcell-09-662191-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/535d/8056019/acadee797383/fcell-09-662191-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/535d/8056019/acadee797383/fcell-09-662191-g001.jpg

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