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Suh, Pann-Ghill
BioSignal Network Lab (BSN)
Research Interests
  • Signal transduction, cancer, metabolism, phospholipase C

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Haloperidol induces calcium ion influx via L-type calcium channels in hippocampal HN33 cells and renders the neurons more susceptible to oxidative stress

Cited 5 times inthomson ciCited 8 times inthomson ci
Title
Haloperidol induces calcium ion influx via L-type calcium channels in hippocampal HN33 cells and renders the neurons more susceptible to oxidative stress
Author
Kim, Hyeon SooYumkham, SanatombiChoi, Jang HyunKim, Eung-KyunKim, Yong SikRyu, Sung HoSuh, Pann-Ghill
Issue Date
2006-08
Publisher
KOREAN SOC MOLECULAR & CELLULAR BIOLOGY
Citation
MOLECULES AND CELLS, v.22, no.1, pp.51 - 57
Abstract
Haloperidol is a classical neuroleptic drug that is still in clinical use and can lead to abnormal motor activity following repeated administration. However, there is little knowledge of how it triggers neuronal impairment. In this study, we report that it induced calcium ion influx via L-type calcium channels and that the elevation of calcium ions induced by haloperidol appeared to render hippocampal cells more susceptible to oxidative stress. Indeed, the level of cytotoxic reactive oxygen species (ROS) and the expression of proapoptotic Bax increased in response to oxidative stress in haloperidol-treated cells, and these effects were inhibited by verapamil, a specific L-type calcium channel blocker, but not by the T-type calcium channel blocker, mibefradil. These findings indicate that haloperidol induces calcium ion influx via L-type calcium channels and that this calcium influx influences neuronal fate.
URI
https://scholarworks.unist.ac.kr/handle/201301/7265
URL
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=33748308814
ISSN
1016-8478
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BIO_Journal Papers
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