Effects of Haloperidol on Ca2+i Change in HIT T-15 Insulinoma Cells / 대한정신약물학회지
Korean Journal of Psychopharmacology
;
: 288-298, 2007.
Article
in Korean
| WPRIM
| ID: wpr-193446
ABSTRACT
OBJECTIVE:
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, which might be linked to the pathogenesis of haloperidol-induced diabetes mellitus.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Calcium
/
Receptors, sigma
/
Diabetes Mellitus
/
KATP Channels
/
Haloperidol
/
Insulinoma
/
Membrane Potentials
Limits:
Animals
Language:
Korean
Journal:
Korean Journal of Psychopharmacology
Year:
2007
Type:
Article
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