Journal article
Aisylu S Gaifullina, J. Lazniewska, E. Gerasimova, Gulshat Burkhanova, Y. Rzhepetskyy, A. Tomin, P. Rivas-Ramírez, Junting Huang, Leos Cmarko, G. Zamponi, G. Sitdikova, N. Weiss
Pain, 2019
Pain, 2019
Semantic Scholar
DOI
PubMed
Video abstract
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APA
Gaifullina, A. S., Lazniewska, J., Gerasimova, E., Burkhanova, G., Rzhepetskyy, Y., Tomin, A., … Weiss, N. (2019). A potential role for T-type calcium channels in homocysteinemia-induced peripheral neuropathy. Pain.
Chicago/Turabian
Gaifullina, Aisylu S, J. Lazniewska, E. Gerasimova, Gulshat Burkhanova, Y. Rzhepetskyy, A. Tomin, P. Rivas-Ramírez, et al. “A Potential Role for T-Type Calcium Channels in Homocysteinemia-Induced Peripheral Neuropathy.” Pain (2019).
MLA
Gaifullina, Aisylu S., et al. “A Potential Role for T-Type Calcium Channels in Homocysteinemia-Induced Peripheral Neuropathy.” Pain, 2019.
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 upon 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 via a PKC-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.
