Kazan Federal University Digital Repository

Homocysteine-induced membrane currents, calcium responses and changes in mitochondrial potential in rat cortical neurons

Show simple item record

dc.contributor.author Abushik P.
dc.contributor.author Karelina T.
dc.contributor.author Sibarov D.
dc.contributor.author Stepanenko Y.
dc.contributor.author Giniatullin R.
dc.contributor.author Antonov S.
dc.date.accessioned 2018-09-18T20:05:02Z
dc.date.available 2018-09-18T20:05:02Z
dc.date.issued 2015
dc.identifier.issn 0022-0930
dc.identifier.uri https://dspace.kpfu.ru/xmlui/handle/net/136342
dc.description.abstract © 2015, Pleiades Publishing, Ltd. Homocysteine, a sulfur-containing amino acid, exerts neurotoxic effects and is involved in the pathogenesis of many neurodegenerative disorders. In contrast to well-studied glutamate excitotoxicity, the mechanism of homocysteine neurotoxicity is not clearly understood. Using wholecell patch-clamp, calcium imaging (fluo-3) and measurements of mitochondrial membrane potential (rhodamine 123), we studied in vitro in cultured rat cortical neurons transmembrane currents, calcium signals and changes in mitochondrial membrane potential induced by homocysteine versus responses induced by NMDA and glutamate. L-homocysteine (50 μM) induced inward currents that were completely blocked by the selective antagonist of NMDA receptors, AP-5. In contrast to NMDA-induced currents, homocysteine-induced currents exhibited a smaller steady-state amplitude. Comparison of calcium responses to homocysteine, NMDA or glutamate demonstrated that in all cortical neurons homocysteine elicited fast oscillatory-type calcium responses, whereas NMDA or glutamate induced a “classical” sustained elevation of intracellular calcium. In contrast to NMDA, homocysteine did not cause a drop in mitochondrial membrane potential at the early stages of its action. However, after its long-term effect, as in cases of NMDA and glutamate, changes in mitochondrial membrane potential arose comparable with its complete drop caused by protonophore FCCP-induced uncoupling of the respiratory chain. Our data suggest that in cultured rat cortical neurons homocysteine at the initial stages of its action induces in vitro neurotoxic effects due to the activation of NMDA-type ionotropic glutamate receptors followed by a massive calcium influx through the channels of these receptors. The long-term effect of homocysteine may lead to mitochondrial dysfuction manifested as a drop in mitochondrial membrane potential.
dc.relation.ispartofseries Journal of Evolutionary Biochemistry and Physiology
dc.subject calcium
dc.subject cortical neurons
dc.subject glutamate
dc.subject homocysteine
dc.subject mitochondrial potential
dc.title Homocysteine-induced membrane currents, calcium responses and changes in mitochondrial potential in rat cortical neurons
dc.type Article
dc.relation.ispartofseries-issue 4
dc.relation.ispartofseries-volume 51
dc.collection Публикации сотрудников КФУ
dc.relation.startpage 296
dc.source.id SCOPUS00220930-2015-51-4-SID84943637565

Files in this item

This item appears in the following Collection(s)

  • Публикации сотрудников КФУ Scopus [24551]
    Коллекция содержит публикации сотрудников Казанского федерального (до 2010 года Казанского государственного) университета, проиндексированные в БД Scopus, начиная с 1970г.

Show simple item record

Search DSpace

Advanced Search


My Account