一氧化氮供体SNP和DEA对培养海马神经元L-型钙电流的影响  

Effects of NO donor SNP and DEA on L-type calcium currents in cultured hippocampal neurons

作　　者：简葵欢[1] 陈明[1] 冯文龙[2] 高天明[1] 

机构地区：[1]南方医科大学神经生物学教研室,广州510515 [2]香港大学医学院生理学系

出　　处：《中华神经医学杂志》2006年第6期550-554,共5页Chinese Journal of Neuromedicine

基　　金：国家基金委与香港研究资助局联合科研基金(30218004);国家自然科学基金(30330240;30125013);教育部长江学者奖励计划资助项目

摘　　要：目的观察NO供体DEA和SNP对大鼠海马培养神经元L-型钙电流的影响并对其机理进行初步探讨。方法L-型钙电流用膜片钳的全细胞模式进行记录。结果DEA和SNP这二种NO供体的主要效应为抑制作用。3 mmol/L DEA可抑制L-型钙电流,当电压去极化至10mV时,电流被抑制了29%。SNP对通道也主要起抑制作用,并且呈现剂量依赖性。当用NEM预处理以阻断S-亚硝化通路后,SNP仍对L-型钙电流产生相似的抑制作用,表明S-亚硝化机制不参与该调控作用。用10μmol/L ODQ预处理以阻断cGMP途径后,SNP仍对通道有抑制作用,表明存在另一种非cGMP通路的抑制性机制。结论上述结果表明,NO供体DEA和SNP对海马神经元L-型钙电流具有抑制作用,其作用机理主要是通过与cGMP途径和S-亚硝化修饰无关的途径。Objective To observe the effects of NO donor SNP and DEA on the modulation of L-type calcium channel currents in cultured rat hippocampal neurons and explore the related possible mechanisms. Methods L-type calcium currents were recorded using the whole cell recording configuration of the patch-clamp technique. Results Both NO donors mainly showed inhibitory effect. 3 mmol/L DEA attenuated the currents by 29% at a depolarizing potential of 10 mV. SNP also showed an inhibition on the channel and such an inhibition was dose-dependent. SNP was used to explore the inhibitory mechanisms. Pretreatment with NEM did not affect the current inhibition induced by SNP, indicating no involvement of S-nitrosylation in the modulation of L-type calcium currents. While pretreated with 10 μmol/L ODQ to block the cGMP pathway, SNP still could inhibit the channel, which suggested another mechanism underlying the inhibition of SNP. Conclusion NO donor SNP and DEA inhibit L-type calcium channel currents in hippocampal neurons via a mechanism other than S-nitrosylation and cGMP pathways.

关 键 词：一氧化氮 L-型钙通道 海马 膜片钳 

分 类 号：Q42[生物学—神经生物学]