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dc.contributor.author | Gaifullina A. | |
dc.contributor.author | Lazniewska J. | |
dc.contributor.author | Gerasimova E. | |
dc.contributor.author | Burkhanova G. | |
dc.contributor.author | Rzhepetskyy Y. | |
dc.contributor.author | Tomin A. | |
dc.contributor.author | Rivas-Ramirez P. | |
dc.contributor.author | Huang J. | |
dc.contributor.author | Cmarko L. | |
dc.contributor.author | Zamponi G. | |
dc.contributor.author | Sitdikova G. | |
dc.contributor.author | Weiss N. | |
dc.date.accessioned | 2020-01-15T22:05:36Z | |
dc.date.available | 2020-01-15T22:05:36Z | |
dc.date.issued | 2019 | |
dc.identifier.uri | https://dspace.kpfu.ru/xmlui/handle/net/156598 | |
dc.description.abstract | Homocysteinemia 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.title | A potential role for T-type calcium channels in homocysteinemia-induced peripheral neuropathy | |
dc.type | Article | |
dc.relation.ispartofseries-issue | 12 | |
dc.relation.ispartofseries-volume | 160 | |
dc.collection | Публикации сотрудников КФУ | |
dc.relation.startpage | 2798 | |
dc.source.id | SCOPUS-2019-160-12-SID85074965976 |