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Glia. 2016 Oct;64(10):1628-45. doi: 10.1002/glia.22967. Epub 2016 Feb 26.

Sodium channels in astroglia and microglia.

Author information

1
Department of Neurology and Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, CT.
2
Rehabilitation Research Center, VA Connecticut Healthcare System, West Haven, CT.

Abstract

Voltage-gated sodium channels are required for electrogenesis in excitable cells. Their activation, triggered by membrane depolarization, generates transient sodium currents that initiate action potentials in neurons, cardiac, and skeletal muscle cells. Cells that have not traditionally been considered to be excitable (nonexcitable cells), including glial cells, also express sodium channels in physiological conditions as well as in pathological conditions. These channels contribute to multiple functional roles that are seemingly unrelated to the generation of action potentials. Here, we discuss the dynamics of sodium channel expression in astrocytes and microglia, and review evidence for noncanonical roles in effector functions of these cells including phagocytosis, migration, proliferation, ionic homeostasis, and secretion of chemokines/cytokines. We also examine possible mechanisms by which sodium channels contribute to the activity of glial cells, with an eye toward therapeutic implications for central nervous system disease. GLIA 2016;64:1628-1645.

KEYWORDS:

EAE; astrocytes; microglia; multiple sclerosis; sodium channels; sodium-calcium exchanger

PMID:
26919466
PMCID:
PMC5730353
DOI:
10.1002/glia.22967
[Indexed for MEDLINE]
Free PMC Article

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