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KMID : 0361520070180050288
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Korean Journal of Psychopharmacology
2007 Volume.18 No. 5 p.288 ~ p.298
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Effects of Haloperidol on [Ca²+]i Change in HIT T-15 Insulinoma Cells
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Kim Min-Hyock
Park Ki-Chang
Jin Se-Young
Kim Dae-Ran
Kim Min-Jeong
Park Kyu-Sang
Kong In-Deok
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Abstract
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Objectives :The purpose of this study was to investigate the effects of haloperidol on [Ca²+]i in hamster insulinoma cells (HIT T-15).
Methods:[Ca²+]i levels were measured by calcium imaging techniques, and membrane potential ionic currents were recorded using conventional patch-clamp methods.
Results:Haloperidol induced a transient [Ca²+]i increase, which was abolished by the removal of extracellular Ca²+ or pretreatment with Ca²+ channel blockers (nimodipine and mibefradil). Haloperidol depolarized the membrane potential and inhibited the ATP-sensitive K+ (KATP) channels. Sigma receptor agonists, (+)-SKF10047 and ifenprodil, induced a transient [Ca²+]i increase similar to haloperidol. BD1047, a sigma receptor antagonist, completely blocked the [Ca²+]i increase induced by haloperidol. Haloperidol inhibited the KCl-induced [Ca²+]i increase and voltage-dependent Ca²+ currents. Sigma receptor agonists [(+)-SKF10047, ifenprodil] also inhibited the KCl-induced [Ca²+]i increase.
Conclusion:Our results suggest that haloperidol induces depolarization, which increases [Ca²+]i by voltage-gated Ca²+ currents via the closing of KATP channels. Haloperidol also inhibits KCl-induced [Ca²+]i increases in the same manner. These effects of haloperidol seemed to be mediated by sigma receptors,
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KEYWORD
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Haloperidol, HIT T-15 cell, [Ca²+]i, Sigma receptor
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