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

Hyeon Soo Kim, Sanatombi Yumkham, Jang Hyun Choi, Eung Kyun Kim, Yong Sik Kim, Sung Ho Ryu, Pann Ghill Suh

Research output: Contribution to journalArticle

10 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)51-57
Number of pages7
JournalMolecules and cells
Volume22
Issue number1
Publication statusPublished - 2006 Aug 31

Keywords

  • Calcium
  • Haloperidol
  • Hippocampus
  • L-type calcium channel
  • Oxidative stress
  • Verapamil

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

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