幼年爪蟾视顶盖神经元微兴奋性突触后电流的一些特性  

Some characteristics of mEPSC in the tectal neurons of juvenile Xenopus

作　　者：王红[1] 蔡浩然[1] 

机构地区：[1]北京大学第一医院中心实验室,北京100034

出　　处：《中国神经科学杂志》2002年第4期708-714,共7页

基　　金：国家自然科学基金 (3 9670 774)资助项目

摘　　要：以微兴奋性突触后电流 (miniatureexcitatorypostsynapticcurrents,mEPSCs)为指标 ,采用盲法膜片电压钳全细胞记录技术 ,研究敏感期内爪蟾视顶盖神经元突触前受体调制突触后mEPSCs的作用。结果发现 ,mEP SCs可以被NMDA受体特异性阻断剂APV和 (或 )AMPA/KA受体特异性阻断剂CNQX所阻断 ,NMDA受体激动剂NMDA可以诱发内向突触后电流。与成年神经元相比 ,未成年动物神经元的mEPSCs的下降相时间较长 ,mEPSCs的NMDA成分较多 ,而AMPA成分较少。尼古丁乙酰胆碱受体激动剂 (carbachol,nicotine和cytisine)可使mEPSCs的频率增加 ,且carbachol使频率增加作用需要Ca2 +介导 ;而乙酰胆碱水解产物choline亦有此作用 ;尼古丁乙酰胆碱受体的竞争性拮抗剂DH β E能够拮抗carbachol诱发的mEPSCs频率增加作用 ;α3β4亚型尼古丁乙酰胆碱受体拮抗剂mecamyllamine不能拮抗carbachol诱发的mEPSCs频率增加作用 ,但在低浓度下对含有α7亚单元尼古丁乙酰胆碱受体起特异拮抗作用的MLA却有这种拮抗作用 ;同时我们还观察到 ,无Ca2 +灌流可以导致巨型PSCs的出现 ,无镁液可以使mEPSCs的下降相延长。结果表明 ,mEPSCs是由NMDA受体和AMPA/KA受体共同介导的 ,尼古丁乙酰胆碱受体以Ca2 +依赖的方式参与了mEPSCs的突触前调制 。The study aimed to investigate the modulation of presynaptic receptor on postsynaptic mEPSCs by measuring miniature excitatory postsynaptic currents (mEPSCs) in Xenopus ' optic tectum during critical peroid. Voltage clamp technique with whole cell mode was used. The results demonstrated that NMDA receptor agonist NMDA could induce depolarized postsynaptic inward going current. AMPA/KA receptor antagonist CNQX could block the rapid component of spontaneous inward going currents,NMDA receptor antagonist APV could block the slow component of spontaneous inward going currents. The mEPSCs underwent developmental changes during the whole critical peroid. Compared with mature neurons, mEPSCs recorded from immature neurons appeared slower decay time. The nicotine acetylcholine agonists (carbachol, cytisine and nicotine) could increase the frequency of mEPSCs. The frequency enhancement of mEPSCs induced by nAChR agonist was calcium dependent. And choline, a product of hydrolyzed acetylcholine, could also increase the frequency of mEPSCs. DH β E, a nAChR competitive antagonist, blocked the increase of mEPSCs frequency induced by carbachol. The α7 subtype of nAChR antagnist MLA blocked the carbachol induced enhancement of mEPSCs frequency. However, mecamyllamine, an α3β4 subtype of nAChR antagonist, could not block the enhancement of mEPSCs induced by carbachol. In conclusion,the mEPSCs are mediated by NMDA and AMPA/KA receptors. It seems that nAChR could presynaptically modulate the mEPSCs, in which α7 subtype of nAChR might be involved. Meanwhile, we found that Ca 2+ free solution could elicit giant PSC. Mg 2+ free solution could prolong the decay time of mEPSCs.

关 键 词：视顶盖 脑片 敏感期 NMDAR 微兴奋性突触后电流 mEPSCs 膜片钳 N型乙酰胆碱受体 MACHR 

分 类 号：Q42[生物学—神经生物学]