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白介素1β抑制培养的大鼠皮层神经元钠电流峰值和动作电位幅度 被引量:2

Interleukin-1β inhibits the amplitudes of voltage-gated Na^+ currents and action potential in cultured cortical neurons of rat
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摘要 白介素1β(interleukin-1β,IL-1β)是重要的促炎细胞因子,在中枢神经系统的生理学和病理学过程中发挥关键作用。电压门控钠通道是可兴奋细胞电学活动的基础,控制神经元的兴奋性和动作电位。最近的研究又显示了IL-1β与电压门控通道之间的相互作用。为考察中枢神经元中IL-1β与电压门控钠通道之间的相互作用,本研究使用10ng/mL的IL-1β处理培养的大鼠皮层神经元24h,通过电压钳技术测定电压门控钠电流,结果表明IL-1β处理抑制钠电流幅度,但不改变其激活和失活性质。与电压钳记录结果相一致,电流钳记录表明IL-1β降低动作电位幅度但不影响阈值。这些结果显示长时间的IL-1β处理可以抑制电压门控钠电流,这种抑制作用减小了动作电位幅度,这可能改变神经元的电学性质、突触传导等基本功能,并提示了IL-1β在神经系统损伤和疾病中作用的新的思路。 Interleukin-1β (IL-1β) is an important proinflammatory cytokine and plays key roles in physiological and pathophysiological processes of central nervous system(CNS).The voltage-gated Na+ channels are essential for electrical properties of excitable cells and control the excitability and action potential(AP) of neurons.Recent studies have showed the relationship between IL-1β and voltage-gated channels.In this work,cultured cortical neurons of rat were treated by 10 ng/mL of IL-1β for 24 h,and then voltage-gated Na+ currents were recorded using voltage-clamp technique.The results indicated that IL-1β reduced the amplitude of Na+ currents without any changes in activation or inactivation properties.The current-clamp recording showed that IL-1β reduced the amplitude of AP but not the threshold.These data indicate that IL-1β inhibits the voltage-gated Na+ currents and the amplitude of AP,and suggest that essential roles of voltage-gated Na+ channels may be changed by IL-1β.New information about effects of IL-1β on injuries and diseases of CNS was provided.
出处 《生理学报》 CAS CSCD 北大核心 2011年第2期131-137,共7页 Acta Physiologica Sinica
基金 supported by the Scientific Research Program of Educational Department of Hebei Province China(No.Z2009109) the Open Funds of the State Key Laboratory of Biomembrane and Membrane Biotechnology Beijing University China
关键词 白介素1Β 皮层神经元 电压门控钠电流 动作电位 interleukin-1β cortical neurons voltage-gated Na+ currents action potential
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  • 1Rothwell N J, Luheshi GN. Functional interactions between presynaptic calcium channels and the neurotransmitter release machinery. Curr Opin Neurobiol2000; 13: 308-314.
  • 2Griffin WS, Mark RE. Interleukin-1 in the genesis and progression of and risk for development of neuronal degeneration in Alzheimer's disease. J Leukoc Biol 2002; 72: 233- 238.
  • 3Petel HC, Boutin H, Allan SM. Interleukin-1 in the brain: Mechanisms of action in acute neurodegeneration. Ann NY Acad Sci 2003; 992: 39-47.
  • 4Rothwell NJ. Interleukin-1 and neuronal injury: Mechanisms, modification, and therapeutic potential. Brain Behav Immun 2003; 17: 152-157.
  • 5Fogal B, Hewett SJ. Interleukin-1 β: a bridge between inflammation and excitotoxicity? J Neurochem 2008; 106:1 23.
  • 6Rijkers K, Majoie H J, Hoogland G, Kenis G, Baets M, Vies JS. The role of interleukin-1 in seizures and epilepsy: A critical review. Exp Neurol 2009; 216: 258-271.
  • 7Li Y, Liu L, Kang J, Sheng JG, Barger SW, Mark RE, Griffin WS. Neuronal-glial interactions mediated by interleukin-1 enhance neuronal acetylcbolinesterase activity and mRNA expression. J Neurosci 2000; 20: 149-155.
  • 8Viviani B, Bartesaghi S, Gardoni F, Vezzani A, Behrens MM, Bartfai T, Binaglia M, Corsini E, Diluca M, Galli CL, Marinovich M. Interleukin-1β enhances NMDA receptormediated intracellular calcium increase through activation of the Src family of kinases. J Neurosci 2003; 23: 8692-8700.
  • 9Ringheim GE, Burgher KL, Heroux JA. Interleukin-6 mRNA expression by cortical neurons in culture: Evidence for neuronal sources of interleukin-6 production in the brain. J Neuroimmunol 1995; 63: 113-123.
  • 10Thorns V, Walter GF, Licastro F. Effects of IL-6 and IL-1β on aFGF expression and excitotoxicity in NT2N cells. J Neuroimmunol 2002; 127: 22-29.

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