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齐翠, 张伟伟, 王飞, 鲍朝飞, 王歆玮, 李霄楠, 余晓青. 2011: 白介素1β对大鼠皮层神经元钠电流的急性作用. 动物学研究, 32(3): 323-328. DOI: 10.3724/SP.J.1141.2011.03323
引用本文: 齐翠, 张伟伟, 王飞, 鲍朝飞, 王歆玮, 李霄楠, 余晓青. 2011: 白介素1β对大鼠皮层神经元钠电流的急性作用. 动物学研究, 32(3): 323-328. DOI: 10.3724/SP.J.1141.2011.03323
QI Cui, ZHANG Wei-Wei, WANG Fei, BAO Chao-Fei, WANG Xin-Wei, LI Xiao-Nan, YU Xiao-Q. 2011: Acute effects of IL-1β on sodium current in cortical neurons of rats. Zoological Research, 32(3): 323-328. DOI: 10.3724/SP.J.1141.2011.03323
Citation: QI Cui, ZHANG Wei-Wei, WANG Fei, BAO Chao-Fei, WANG Xin-Wei, LI Xiao-Nan, YU Xiao-Q. 2011: Acute effects of IL-1β on sodium current in cortical neurons of rats. Zoological Research, 32(3): 323-328. DOI: 10.3724/SP.J.1141.2011.03323

白介素1β对大鼠皮层神经元钠电流的急性作用

Acute effects of IL-1β on sodium current in cortical neurons of rats

  • 摘要: 白介素1β(Interleukin-1β, IL-1β)是重要的促炎细胞因子, 在多种中枢神经系统的损伤和疾病过程中发挥关键作用。电压门控的钠通道是神经元中最重要的离子通道之一, 是产生再生性动作电位的基础, 决定了神经元的兴奋性等电学性质, 也与多种中枢疾病过程相关。然而, 现在还没有直接关于IL-1β与中枢钠通道的相互关系的研究。在该研究中, 使用全细胞膜片钳记录测定了IL-1β对培养的皮层神经元钠电流的急性作用, 并分析了由此对动作电位的影响。结果显示, IL-1β对钠电流幅度只有较小的抑制, 而显著降低钠通道的半激活电压, 不改变激活的斜率因子和失活性质, 这个作用引起动作电位阈值显著降低。这些结果提示在损伤和疾病过程中, 快速释放的IL-1β可能会增加神经元兴奋性, 从而恶化神经损伤过程。

     

    Abstract: Interleukin-1β (IL-1β) is an important proinflammatory cytokine that plays a key role in injuries and diseases of the central nervous system (CNS). The voltage-gated Na+channel is the most important ion channel of neurons, and is essential for regenerative action potential (AP). The Na+ channel also contributes to many diseases of the brain. However, relations between IL-1β and central Na+ channels remain unreported. In this study, whole cell patch-clamp recording was used to investigate the acute effects of IL-1β (10 ng/mL) on voltage-dependent Na+ currents and AP of cultured cortical neurons from rats. Results showed that the half-activation voltage of Na+ channels and the threshold of AP, but not the amplitude, slope factor of activation, and inactivation properties, were affected by IL-1β. These data suggest that increased IL-1β in injury and disease may upregulate the excitability of neurons, and thereby exacerbate neurotoxicity.

     

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