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University of Texas Health Science Center at San Antonio

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Cell Reports, Volume 36, Issue 10, 7 September 2021, 109653 | https://doi.org/10.1016/j.celrep.2021.109653 SCN2A contributes to oligodendroglia excitability and development in the mammalian brain

Elizabeth Gould¹, Jun Hee Kim^1,2,*

¹Department of Cellular and Integrative Physiology, University of Texas Health Science Center, San Antonio, TX 78229, USA
²Lead contact

^*Corresponding author

Abstract

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.

Keywords : oligodendrocyte, sodium channel, development, SCN2A, single-cell transcriptomics

논문정보

형식Research article
게재일2021년 09월 (BRIC 등록일 2021-09-14)
연구진국외 연구진
분야 의약학 > 신경의학

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