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钾-氯离子转运体2仅在中枢神经系统表达,具有神经元特异性。KCC2在维持神经元内氯离子的浓度发挥重要的作用,它主要调节细胞内Cl-的外向流量,使神经元内氯离子浓度低于它的电化学平衡单位,使γ-氨基丁酸能神经元发生超级化的突触后抑制性反应。KCC2在癫痫发病过程中具有重要的作用,在神经元内KCC2的表达减少,使细胞内Cl-增加,改变了神经元内Cl-的稳态,改变γ-氨基丁酸的突触后抑制性电位,GABA能反应向去极化方向转换,促进癫痫发生与发展。
Potassium-chloride ion transporter 2 is expressed only in the central nervous system and is neuron specific. KCC2 plays an important role in maintaining the concentration of chloride ion in neurons. It mainly regulates the outward flux of Cl- in neurons so that the concentration of chloride ion in neurons is lower than its electrochemical equilibrium unit. KCC2 activates γ-aminobutyric acid Metaphase super-post-synaptic inhibitory response. KCC2 plays an important role in the pathogenesis of epilepsy. The decrease of KCC2 expression in neurons leads to the increase of intracellular Cl-, changes the Cl- homeostasis in neurons and changes the post-synaptic inhibitory effect of GABA Potential, GABA can respond to depolarization direction conversion, and promote the occurrence and development of epilepsy.