BK、SK通道参与慢性损伤坐骨神经异常自发放电节律的调控  

Calcium-activated potassium channels participate in modifying ectopic discharges of injured nerves in CCI model rat

作　　者：路美玲[1] 李建宁[1] 魏春玲[1] 刘一辉[1] 任维[1] 

机构地区：[1]陕西师范大学生命科学学院,陕西西安710062

出　　处：《陕西师范大学学报（自然科学版）》2014年第1期70-75,共6页Journal of Shaanxi Normal University：Natural Science Edition

基　　金：国家自然科学基金资助项目(30900443)

摘　　要：通过运用相对特异的钙激活钾通道阻断剂蝎毒和蜂毒明肽分别阻断BK和SK通道,观察对损伤神经自发放电模式的影响,并将其与非特异性钾通道阻断剂四乙基铵的作用进行比较,以揭示参与调节放电节律的钙激活钾离子通道的亚型.结果显示,蝎毒和蜂毒明肽均可以使放电节律呈现分岔转迁.这些结果提示在坐骨神经的损伤区表达有BK与SK通道,并可能参与调控损伤区神经纤维的自发放电.Previous studies on ectopic firing of injured nerves in the chronic constriction injury （CCI） model indicated that calcium-activated potassium channels play a key role, but the direct pharmacological evidence has not been reported. This study examined the effect of TEA and rela- tively specific calcium-activated potassium channel blockers IBTX and Apamin on spontaneous fir- ing of injury nerves in CCI model rats. The results showed that both IBTX and Apamin could lead to bifurcation scenarios, indicating that the BK and SK channels are involved in the regula- tion of spontaneous firing of injured nerves. The results imply that calcium-activated potassium channels may exist in injured nerves in CCI model, and may be involved in regulation of spontane- ous firing of injured nerves.

关 键 词：慢性结扎损伤模型 自发放电 钙激活钾通道 

分 类 号：Q423[生物学—神经生物学]