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Altered neuronal expression of TASK1 and TASK3 potassium channels in rodent and human autoimmune CNS inflammation.

Abstract：

:Multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis (EAE) are characterized by T cell-mediated autoimmune inflammation of the central nervous system (CNS) leading to oligodendrocyte loss and demyelination accompanied by neuronal cell death. Neuronal TWIK-related acid-sensitive potassium (TASK) channels allow the regulated efflux of potassium ions. These channels might either protect neurons in the inflamed CNS by modulating electrical excitability or even contribute to inflammatory neurodegeneration mediating intracellular potassium depletion. Using a combination of in-situ-hybridisation and immunofluorescence staining, we found increased neuronal expression of TASK1 and TASK3 channels in the optic nerve and decreased expression in the spinal cord and thalamus of rats undergoing MOG-induced EAE. Inflammatory plaques of human MS patients displayed profoundly lowered expression of both TASK isoforms. Thus, regulated expression of TASK channels might contribute to a molecular switch between death and survival of neurons in autoimmune CNS inflammation.

journal_name

Neurosci Lett

journal_title

Neuroscience letters

authors

Meuth SG,Kanyshkov T,Melzer N,Bittner S,Kieseier BC,Budde T,Wiendl H

doi

10.1016/j.neulet.2008.09.038

subject

Has Abstract

pub_date

2008-12-03 00:00:00

pages

133-8

issue

2-3

eissn

0304-3940

issn

1872-7972

pii

S0304-3940(08)01288-3

journal_volume

446

pub_type

杂志文章

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