GABAergic网络在神经发育和脑疾病中对髓鞘再生的研究进展  

Advances of studies on myelin regeneration by GABAergic networks in neurodevelopment and brain diseases

作　　者：范晓迪[1] 张业昊 刘建勋[1] FAN Xiao-di;ZHANG Ye-hao;LIU Jian-xun(Beijing Key Laboratory of Pharmacology of Chinese Materia Medica,Institute of Basic Medical Sciences,Xiyuan Hospital of China Academy of Chinese Medical Sciences,Beijing 100091,China)

机构地区：[1]中国中医科学院西苑医院基础医学研究所,中药药理北京市重点实验室,北京100091

出　　处：《中国药理学通报》2024年第5期801-806,共6页Chinese Pharmacological Bulletin

基　　金：中国中医科学院科技创新工程项目(No CI2021A04617,CI2021A01304);国家自然科学基金资助项目(No 82104444,8203000944);中国中医科学院优秀青年科技人才培养专项(No ZZ15-YQ-008)。

摘　　要：少突胶质细胞前体细胞(oligodendrocyte precursor cells,OPCs)分化为成熟的少突胶质细胞(oligodendrocytes,OLs)是中枢神经系统轴突髓鞘形成和脱髓鞘疾病髓鞘再生的关键事件。研究表明,神经递质γ-氨基丁酸(γ-aminobutyric acid,GABA)、GABAergic突触及其网络调控对少突神经胶质细胞的增殖、分化、迁移及髓鞘形成具有重要的调节作用。因此,该文总结了近些年关于GABA及其受体在少突胶质细胞谱系中发挥的生物学功能,GABAergic中间神经元与OPCs之间的交互作用及其介导髓鞘形成的网络调控和未来潜在的候选药物的研究。基于此了解控制OLs分化机制对于确定促进髓鞘修复的治疗策略至关重要,围绕GABAergic的研究可能对开发脱髓鞘疾病的新型修复疗法具有潜在意义。Differentiation of oligodendrocyte precursor cells(OPCs)into mature oligodendrocytes(OLs)is a key event for axonal myelination in the central nervous system(CNS).Stud-ies have shown that neurotransmitters like GABA,GABAergic synapses and network regulation play important roles in the pro-liferation,differentiation,migration and myelination of oligoden-drocytes.Therefore,the paper reviews recent studies on the biological functions of GABA and its receptors in oligodendrocyte lineages,the interaction between GABAergic interneurons and OPCs,the network regulation of GABAergic interneurons mediating myelination,and potential future drug candidates.Based on this,understanding the mechanisms that control OLs differentiation is essential for identifying therapeutic strategies that promote myelin repair,and research surrounding GABAergic may have potential implications for the development of novel repair therapies for demyelinating diseases.

关 键 词：γ-氨基丁酸 GABA能网络 少突胶质细胞 中间神经元 髓鞘再生 神经发育与疾病 

分 类 号：R322.81[医药卫生—人体解剖和组织胚胎学] R329.28[医药卫生—基础医学] R338.1R971.4R971.9