摘要：

Theiler'surine encephalomyelitis virus (TMEV) induces demyelination inusceptibletrainsficehroughD4~+h1ell-mediated immunopathological process.MEV infection producesyndrome inicehatesemblesultipleclerosis. Inhis work, weocusednhe increased expressionfhe genes encoding voltage-gateda~(2+)hannelubunits inJL/Jousestrocytes infected inulture witheAntrainfMEV.ffymetrix DNAurine genome74v2 DNAicroarrayybridized withRNAromock-ndMEV-infectedstrocytesevealedhepregulationfourequences encodinga~(2+)-bindingnda~(2+)hannelubunit proteins.he DNAybridizationesults wereurther validatedsingonventionalT-PCRnd quantitativeT-PCR, demonstratinghe increased expressionfRNA encodinghannelubunit proteins. Westernlottinglsohowedhe increasedynthesisf L-nd N-typehannelubunitpecific proteinsfter infection.heeduced expressionndheunctionalpregulationfunctional voltage-gateda~(2+)hannels inock-andMEV-infectedells,espectively, was demonstratedsing voltagelamp experiments.MEV infection inousestrocytes induceda~(2+)urrent with density proportionalohemountf viral particlessedor infection.hesefa~(2+)hannellockers, nimodipinendmega-cono-toxin-GVIA,howedhatothunctional L-nd N-typea~(2+)hannels werepregulated in infectedstrocytes.hepregulationfa~(2+)hannels instrocytesfterMEV infection provides insight intoheolecular processesnd potentialolefstrocytea~(2+) dysregulation inhe pathophysiologyf encephalomyelitisnd is importantorhe developmentf novelherapeutictrategies leadingo preventionf neurodegeneration.

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