Abstract
Immature oligodendrocytes (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 examined the molecular profile of spiking OLs using single-cell transcriptomics paired with whole-cell patch-clamp recordings. SCN2A, which encodes the channel Nav1.2, was uniquely expressed in spiking OLs in both the brainstem and cerebellum, and across species in mice and the non-human primate, Olive baboon. Spiking OLs expressed genetic markers of both oligodendrocyte progenitor cells (OPCs) and pre-myelinating OLs, indicating they belong to a transitional stage during differentiation. The genetic deletion of SCN2A reduced the Nav current-expressing OL population and eliminates spiking OLs, indicating that SCN2A is essential for spiking in OLs. The absence of SCN2A did not impact global OL proliferation, but disrupted the maturation of a subpopulation of OLs, suggesting a distinct role for Nav1.2 in regulating OL development.
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