Chronic haloperidol increases voltage-gated Na currents in mouse cortical neurons |
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Authors: | Weiqiang Chen Fangfang Zhu Jingfang Guo Jiangtao Sheng Wenli Li Xiangfeng Zhao Gefei Wang Kangsheng Li |
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Affiliation: | 1. Department of Neurosurgery, First Affiliated Hospital, Shantou University Medical College, 57 Changping Road, Shantou, Guangdong 515041, China;2. Department of Microbiology and Immunology, Key Immunopathology Laboratory of Guangdong Province, Shantou University Medical College, 22 Xinling Road, Shantou, Guangdong 515041, China |
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Abstract: | Typical antipsychotics are characterized by extrapyramidal syndrome (EPS). Previous studies demonstrated that typical antipsychotics could inhibit neuronal voltage-gated sodium channel (VGSC). However, EPS typically emerge only upon prolonged exposure. As a result, we examined effects of haloperidol, a prototype typical antipsychotic, on neuronal VGSC upon incubation for varying duration. Briefly, VGSC currents were activated and recorded using a whole-cell patch-clamp technique in primary culture of mouse cortical neurons. VGSC activity was inhibited by acute haloperidol exposure (for minutes), but enhanced in a time- and concentration-dependent manner by chronic haloperidol exposure (for hours). The effects of chronic haloperidol were associated with increased expression of VGSC subunits as well as corresponding electrophysiological channel properties. In summary, we found enhanced VGSC currents upon chronic haloperidol exposure in cortical neurons in contrast to inhibition by acute haloperidol exposure. Such a results may contribute to EPS of typical antipsychotics. |
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Keywords: | Haloperidol Voltage-gated sodium channels Cortical neurons Patch-clamp recording Bromocriptine BDNF |
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