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目的了解急性炎性脱髓鞘大鼠模型周围神经轴膜离子通道的变化及其对神经功能的影响。方法使用实验性变态反应性神经炎(EAN)大鼠模型,观察周围神经钠、钾离子通道在病程中的变化,结合神经组织学、神经电生理和临床症状,分析轴膜离子通道与神经传导功能的关系。结果轴膜离子通道在免疫后第9d EAN发病时即明显减少,此后2周内迅速消失。随之是缓慢的恢复过程,但直至免疫后85d,临床症状消失后数周仍未恢复至正常水平。病程中钠、钾通道的变化基本一致,且与结旁段髓鞘的变化密切相关。电生理指标在急性期(免疫后9~23d)与神经结构损害保持一致,动作电位波幅部分反应了轴膜离子通道的水平。结论轴膜离子通道异常是导致疾病起始阶段临床症状的直接原因之一,是病变过程中较易受损且较难恢复的结构部件,其在周围神经的准确定位和维护与特定的结旁段髓鞘结构紧密关联。
Objective To investigate the changes of the ion channels in the peripheral nerve axis of acute inflammatory demyelination rats and their effects on neurological function. Methods The rat model of experimental allergic neuritis (EAN) was used to observe the changes of sodium and potassium channels in peripheral nerves during the course of the disease. Combined with neurohistology, electrophysiology and clinical symptoms, the effects of axial channel ion channels and nerve conduction Functional relationship. Results Axon membrane ion channels significantly decreased at the onset of EAN on day 9 after immunization, and disappeared rapidly within 2 weeks. Followed by a slow recovery process, but up to the 85th day after immunization, the clinical symptoms did not recover to normal levels within weeks. During the course of sodium and potassium channel changes are basically the same, and the changes in the myelin adjacent knot is closely related. Electrophysiological indicators in the acute phase (9 ~ 23d after immunization) consistent with the damage to the nerve structure, the action potential amplitude of the axial response of the axial membrane ion channel level. Conclusion The abnormality of axial membrane ion channels is one of the direct causes of the clinical symptoms in the initial stage of the disease. It is a structural component that is more easily damaged and difficult to be recovered in the process of lesion. The accurate positioning and maintenance of the peripheral nerves and the specific junction Para-myelin structure is closely related.