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A potential role for T-type calcium channels in homocysteinemia-induced peripheral neuropathy

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dc.contributor.authorGaifullina, A.S.
dc.contributor.authorLazniewska, J.
dc.contributor.authorGerasimova, E.V.
dc.contributor.authorBurkhanova, G.F.
dc.contributor.authorRzhepetskyy, Y.
dc.contributor.authorTomin, A.
dc.contributor.authorRivas Ramirez, P.
dc.contributor.authorHuang, J.
dc.contributor.authorCmarko, L.
dc.contributor.authorZamponi, G.W.
dc.contributor.authorSitdikova, G.F.
dc.contributor.authorWeiss, N.
dc.date.issued2019
dc.description.abstractHomocysteinemia is a metabolic condition characterized by abnormally high level of homocysteine in the blood and is considered to be a risk factor for peripheral neuropathy. However, the cellular mechanisms underlying toxic effects of homocysteine on the processing of peripheral nociception have not yet been investigated comprehensively. Here, using a rodent model of experimental homocysteinemia, we report the causal association between homocysteine and the development of mechanical allodynia. Homocysteinemia-induced mechanical allodynia was reversed on pharmacological inhibition of T-type calcium channels. In addition, our in vitro studies indicate that homocysteine enhances recombinant T-type calcium currents by promoting the recycling of Cav3.2 channels back to the plasma membrane through a protein kinase C–dependent signaling pathway that requires the direct phosphorylation of Cav3.2 at specific loci. Altogether, these results reveal an unrecognized signaling pathway that modulates the expression of T-type calcium channels, and may potentially contribute to the development of peripheral neuropathy associated with homocysteinemia.
dc.identifier.citationPain, 2019; 160(2):2798-2810
dc.identifier.doi10.1097/j.pain.0000000000001669
dc.identifier.issn0304-3959
dc.identifier.issn1872-6623
dc.identifier.urihttps://hdl.handle.net/11541.2/144464
dc.language.isoen
dc.publisherLippincott Williams & Wilkins
dc.relation.fundingInstitute of Organic Chemistry and Biochemistry
dc.relation.fundingRussian Science Foundation
dc.relation.fundingCanadian Institutes of Health Research
dc.rightsCopyright 2019 International Association for the Study of Pain
dc.source.urihttps://dx.doi.org/10.1097/j.pain.0000000000001669
dc.subjecthomocysteinemia
dc.subjecthomocysteine
dc.subjectpain
dc.subjectallodynia
dc.subjectcalcium channel
dc.subjectT-type channel
dc.subjectCav3.2
dc.titleA potential role for T-type calcium channels in homocysteinemia-induced peripheral neuropathy
dc.typeJournal article
pubs.publication-statusPublished
ror.mmsid9916440505201831

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