中国疼痛医学杂志
中國疼痛醫學雜誌
중국동통의학잡지
CHINESE JOURNAL OF PAIN MEDICINE
2009年
4期
236-239
,共4页
离子型谷氨酸受体%易化%脊髓背角%长时程增强%电针
離子型穀氨痠受體%易化%脊髓揹角%長時程增彊%電針
리자형곡안산수체%역화%척수배각%장시정증강%전침
Ionotropic glutamate receptors%Facilitated%Spinal dorsal horn%Long-term potentiation%Electroaeupuncture
目的:观察电针对离子型谷氨酸受体(iGluRs)激动剂易化脊髓背角神经元而形成的长时程增强(LTP)的抑制作用,并探讨其机制.方法:大鼠脊髓L4/L5节段细胞外记录脊髓背角C-纤维诱发场电位的LTP.iGluRs激动剂NMDA或[±]-AMPA HBr 40pg鞘内给药(i.t.)易化脊髓背角神经元;对照组i.t.生理盐水2μl.2 Hz,1 mA电针(EA)环跳和委中穴.观察电针对iGluRs激动剂i.t.易化的LTP的抑制作用.结果:对照组低强度强直刺激(HFS)前、后脊髓背角LTP)的变化率无统计学差异;i.t.NMDA或[±]-AMPA HBr后低强度HFS,可引起显著的LTP,与对照组比较P<O.01;先EA然后i.t.NMDA或[±]-AMPA HBr和低强度HFS,LTP被显著抑制(P<0.01);先i.t.iGluRs激动剂和低强度HFS诱导出LTP再EA,也可显著抑制已形成的LTP(P<0.05).结论:低频低强度电针,可抑制iGluRs激动剂易化的脊髓C纤维诱发场电位LTP的形成和维持.提示低频电针可降低脊髓背角神经元的异常兴奋性,此突触后机制可能是电针干预神经病理痛的作用机制之一.
目的:觀察電針對離子型穀氨痠受體(iGluRs)激動劑易化脊髓揹角神經元而形成的長時程增彊(LTP)的抑製作用,併探討其機製.方法:大鼠脊髓L4/L5節段細胞外記錄脊髓揹角C-纖維誘髮場電位的LTP.iGluRs激動劑NMDA或[±]-AMPA HBr 40pg鞘內給藥(i.t.)易化脊髓揹角神經元;對照組i.t.生理鹽水2μl.2 Hz,1 mA電針(EA)環跳和委中穴.觀察電針對iGluRs激動劑i.t.易化的LTP的抑製作用.結果:對照組低彊度彊直刺激(HFS)前、後脊髓揹角LTP)的變化率無統計學差異;i.t.NMDA或[±]-AMPA HBr後低彊度HFS,可引起顯著的LTP,與對照組比較P<O.01;先EA然後i.t.NMDA或[±]-AMPA HBr和低彊度HFS,LTP被顯著抑製(P<0.01);先i.t.iGluRs激動劑和低彊度HFS誘導齣LTP再EA,也可顯著抑製已形成的LTP(P<0.05).結論:低頻低彊度電針,可抑製iGluRs激動劑易化的脊髓C纖維誘髮場電位LTP的形成和維持.提示低頻電針可降低脊髓揹角神經元的異常興奮性,此突觸後機製可能是電針榦預神經病理痛的作用機製之一.
목적:관찰전침대리자형곡안산수체(iGluRs)격동제역화척수배각신경원이형성적장시정증강(LTP)적억제작용,병탐토기궤제.방법:대서척수L4/L5절단세포외기록척수배각C-섬유유발장전위적LTP.iGluRs격동제NMDA혹[±]-AMPA HBr 40pg초내급약(i.t.)역화척수배각신경원;대조조i.t.생리염수2μl.2 Hz,1 mA전침(EA)배도화위중혈.관찰전침대iGluRs격동제i.t.역화적LTP적억제작용.결과:대조조저강도강직자격(HFS)전、후척수배각LTP)적변화솔무통계학차이;i.t.NMDA혹[±]-AMPA HBr후저강도HFS,가인기현저적LTP,여대조조비교P<O.01;선EA연후i.t.NMDA혹[±]-AMPA HBr화저강도HFS,LTP피현저억제(P<0.01);선i.t.iGluRs격동제화저강도HFS유도출LTP재EA,야가현저억제이형성적LTP(P<0.05).결론:저빈저강도전침,가억제iGluRs격동제역화적척수C섬유유발장전위LTP적형성화유지.제시저빈전침가강저척수배각신경원적이상흥강성,차돌촉후궤제가능시전침간예신경병리통적작용궤제지일.
Objective:To observe the inhibitive effects of electroacupuncture(EA)on long-term potentia- tion(LTP)of C-fiber evoked potentials in the spinal dorsal horn facilitated by excitomotor of NMDA or AMPA receptors,and explore the analgesia mechanism of acupuncture in neuropathic pain.Methods: Sprague-Dawley rats were divided into 7 groups:control,NMDA(NMDA)IntratheCal administration(i. t.),AMPA([±]-AMPA HBr)i.t.,EA+NMDA i.t.,EA+AMPA i.t.,NMDA i.t.+EA,and AMPA i.t+EA.The rats were fixed on stereotaxic instrument after anesthesia.C-fiber evoked field potentials in the spinal dorsal horn(L4/L5)were recorded by extracellular recording.The test stimulus was given in single pulse with 2mA,0.5ms,100Hz,5min each once on the sciatic nerve.The lower intensity high- frequency train plus stimulus(HFS)wag given in 4 trains of 1 S duration at 10s intervals with 2mA,0. 5ms,lOOHz on same place.The NMDA or[±]-AMPA HBr(40pg)was injected with i.t.,to excite the related receptor.On GB30 and BL40,EA Wag acupunctured with 1mA,2Hz,30min.Results:In the con- trol,the variation rate of evoked potentials showed no significant differences compared with before or after HFS.After excitomotor i.t then lower intensity HFS.the LTP was induced significantly and com- pared with control(P<0.01).The exeitomotor i.t.and HFS after EA,the LTP was inhibited markedly (P<0.01).After the LTP was steady kept lhr induced by the excitomotor i.t.and HFS,the EA was operated.In NMDA i.t.+EA,LTP was inhibited markedly(P<0.01);In AMPA i.t.+EA,the LTP was step down significantly(P<O.05).Conclusions:These data suggest that the development and retain of LTP on spinal dorsal hom to facilitated by excitomotor of iGluRs WaS inhibited by EA.The results indi- cate that the abnormal excitability of neuron in the spinal dorsal horn with neuropathic pain Was inhibited by EA,which might be the postsynaptic mecharism underlying EA analgesia.