中华神经医学杂志
中華神經醫學雜誌
중화신경의학잡지
CHINESE JOURNAL OF NEUROMEDICINE
2008年
6期
562-566
,共5页
张健%李梅%李享元%李之望%赵斌%吴红玲%苏卓娃%庞红
張健%李梅%李享元%李之望%趙斌%吳紅玲%囌卓娃%龐紅
장건%리매%리향원%리지망%조빈%오홍령%소탁왜%방홍
酸敏感离子通道%H+-门控电流%P物质%三叉神经节%调制
痠敏感離子通道%H+-門控電流%P物質%三扠神經節%調製
산민감리자통도%H+-문공전류%P물질%삼차신경절%조제
Acid-sensing ion channels%Proton-gated current%Substance P%Trigeminal ganglion%Modulation
目的 探讨P物质(SP)对大鼠三叉神经节(TG)神经元膜H+-门控电流的调制作用及其机制.方法 急性分离TG神经元,通过排管快速换液装置行胞外给药,电极内灌药行胞内透析后,采用全细胞膜片钳技术记录神经元膜H+-门控电流.结果 依照我们在背根神经节(DRG)神经元分类的方式,同样可将TG神经元H+-门控电流也分为四型,即T-型、S-型、B-型、O-型;共加SP和H+能浓度依赖性增强S-型H+-门控电流,SP受体拮抗剂GR82334不能阻断此作用;共加SP和H+能增强B-型H+-门控电流,GR82334和胞内透析GDP-β-S能阻断SP对B-型H+-门控电流的这一增强作用,而预加SP则抑制B-型H+-门控电流,并以短暂成分尤为明显,此抑制效应不能被GR82334阻断.结论 SP对H+-门控电流的调制依ASIC亚基组成不同,其作用机制有所不同:S-型H+-门控电流的ASIC分子膜外结构上可能存在SP的别构位点.
目的 探討P物質(SP)對大鼠三扠神經節(TG)神經元膜H+-門控電流的調製作用及其機製.方法 急性分離TG神經元,通過排管快速換液裝置行胞外給藥,電極內灌藥行胞內透析後,採用全細胞膜片鉗技術記錄神經元膜H+-門控電流.結果 依照我們在揹根神經節(DRG)神經元分類的方式,同樣可將TG神經元H+-門控電流也分為四型,即T-型、S-型、B-型、O-型;共加SP和H+能濃度依賴性增彊S-型H+-門控電流,SP受體拮抗劑GR82334不能阻斷此作用;共加SP和H+能增彊B-型H+-門控電流,GR82334和胞內透析GDP-β-S能阻斷SP對B-型H+-門控電流的這一增彊作用,而預加SP則抑製B-型H+-門控電流,併以短暫成分尤為明顯,此抑製效應不能被GR82334阻斷.結論 SP對H+-門控電流的調製依ASIC亞基組成不同,其作用機製有所不同:S-型H+-門控電流的ASIC分子膜外結構上可能存在SP的彆構位點.
목적 탐토P물질(SP)대대서삼차신경절(TG)신경원막H+-문공전류적조제작용급기궤제.방법 급성분리TG신경원,통과배관쾌속환액장치행포외급약,전겁내관약행포내투석후,채용전세포막편겸기술기록신경원막H+-문공전류.결과 의조아문재배근신경절(DRG)신경원분류적방식,동양가장TG신경원H+-문공전류야분위사형,즉T-형、S-형、B-형、O-형;공가SP화H+능농도의뢰성증강S-형H+-문공전류,SP수체길항제GR82334불능조단차작용;공가SP화H+능증강B-형H+-문공전류,GR82334화포내투석GDP-β-S능조단SP대B-형H+-문공전류적저일증강작용,이예가SP칙억제B-형H+-문공전류,병이단잠성분우위명현,차억제효응불능피GR82334조단.결론 SP대H+-문공전류적조제의ASIC아기조성불동,기작용궤제유소불동:S-형H+-문공전류적ASIC분자막외결구상가능존재SP적별구위점.
Objective To investigate the modulatory effect of substance P (SP) on proton-gated current in the membrane of rat trgeminal ganglion (TG) neurons and its underlying mechanism. Methods Neurons were isolated mechanically and enzymatically from TG of rat. Whole-cell patch clamp technique was used for recording the proton-gated current in freshly isolated neurons. Results Proton-gated currents recorded from rat TG neurons could be classified into 4 distinct types: T-type, S-type, B-type and O-type in the present study. Co-application of SP and proton potentiated S-type proton-gated currents in a concentration-dependent manner, and the potentiation was not blocked by SP receptor antagonist, GR82334; co-application of SP and proton potentiated B-type proton-gated currents, and GR82334 and intracellular dialysis of GDP-β-S blocked the potentiation of SP. Pre-application of SP inhibited B-type proton-gated current, especially the transient component. The inhibition could not be reversed by pretreatment wit-h GR82334. Conclusions The mechanisms of modulation of proton-gated current by SP is associated with the difference of their makeup of subunits of acid-sensing ion channels (ASICs), and there may be an allosteric position of SP in the outside framework of ASICs in neuronal membrane.