SCN2A contributes to oligodendroglia excitability and development in the mammalian brain.

SCN2A contributes to oligodendroglia excitability and development in the mammalian brain.
复制标题

DOI:
10.1016/j.celrep.2021.109653
复制
发表时间:
2021-09-07
期刊:
影响因子:
8.8
通讯作者:
Kim JH
Kim JH
中科院分区:
生物学1区
文献类型:
--
作者:
Gould E;Kim JH

文献摘要

参考文献

被引文献

相似文献

尖峰未成熟少突胶质细胞 (OL),称为尖峰 OL,表达电压激活的 Na+ 通道 (Nav) 和 K+ (Kv) 通道,赋予 OL 亚群产生 Nav 驱动尖峰的能力。在这项研究中,我们利用单细胞转录组学与全细胞膜片钳记录配对,研究了尖峰 OL 的分子特征。 SCN2A 编码通道 Nav1.2,在小鼠和橄榄狒狒的脑干和小脑的尖峰 OL 中特异性表达。尖峰 OL 表达 OL 祖细胞 (OPC) 和髓鞘形成前 OL 的谱系标记,表明它们属于分化过程中的过渡阶段。 SCN2A 的缺失减少了表达 Nav 电流的 OL 群体并消除了尖峰 OL,表明 SCN2A 对于 OL 中的尖峰至关重要。 SCN2A 的缺失不会影响整体 OL 增殖,但会破坏 OL 亚群的成熟,表明 Nav1.2 参与 OL 谱系细胞及其发育的异质性。 Gould 和 Kim 使用单细胞转录组学与全细胞膜片钳记录配对,证明由 SCN2A 编码的 Nav1.2 通道赋予未成熟少突胶质细胞 (OL) 亚群的尖峰能力,并在 OL 成熟中发挥重要作用。
Spiking immature oligodendrocytes (OLs), referred to as spiking OLs, express voltage-activated Na+ channels (Nav) and K+ (Kv) channels, endowing a subpopulation of OLs with the ability to generate Nav-driven spikes. In this study, we investigate the molecular profile of spiking OLs, using single-cell transcriptomics paired with whole-cell patch-clamp recordings. SCN2A, which encodes the channel Nav1.2, is specifically expressed in spiking OLs in the brainstem and cerebellum, both in mice and in Olive baboons. Spiking OLs express lineage markers of OL progenitor cells (OPCs) and pre-myelinating OLs, indicating they belong to a transitional stage during differentiation. Deletion of SCN2A reduces the Nav current-expressing OL population and eliminates spiking OLs, indicating that SCN2A is essential for spiking in OLs. Deletion of SCN2A does not impact global OL proliferation but disrupts maturation of a subpopulation of OLs, suggesting that Nav1.2 is involved in heterogeneity in OL lineage cells and their development. Using single-cell transcriptomics paired with whole-cell patch-clamp recordings, Gould and Kim demonstrate that Nav1.2 channels, encoded by SCN2A, endow a subpopulation of immature oligodendrocytes (OLs) with the ability to spike, and serve an essential role in OL maturation.
DOI: 10.1038/s41467-017-00688-0
发表时间: 2017-09-15
影响因子: 16.6
作者:
Berret E;Barron T;Xu J;Debner E;Kim EJ;Kim JH
通讯作者: Kim JH
DOI: 10.1523/jneurosci.6000-09.2010
发表时间: 2010-03-10
期刊: The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子: --
作者:
De Biase LM;Nishiyama A;Bergles DE
通讯作者: Bergles DE
声音诱发的活动会影响梯形体内脑干轴突的髓鞘形成。
DOI: 10.1523/jneurosci.3728-16.2017
发表时间: 2017-08-23
期刊: The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子: --
作者:
Sinclair JL;Fischl MJ;Alexandrova O;Heβ M;Grothe B;Leibold C;Kopp-Scheinpflug C
通讯作者: Kopp-Scheinpflug C
DOI: 10.1016/j.devcel.2018.07.005
发表时间: 2018-08-20
期刊: Developmental cell
影响因子: 11.8
作者:
Marques S;van Bruggen D;Vanichkina DP;Floriddia EM;Munguba H;Väremo L;Giacomello S;Falcão AM;Meijer M;Björklund ÅK;Hjerling-Leffler J;Taft RJ;Castelo-Branco G
通讯作者: Castelo-Branco G
DOI: 10.1016/j.brainres.2015.09.010
发表时间: 2016-05-01
期刊: Brain research
影响因子: 2.9
作者:
Larson VA;Zhang Y;Bergles DE
通讯作者: Bergles DE