【摘要】：目的研究大鼠脊髓背角膠狀質(zhì)(SG)神經(jīng)元的去極化反跳及調(diào)控機制,以期對去極化反跳相關(guān)疾病的臨床治療提供參考。方法選取3~5周齡SD大鼠,制作離體脊髓縱切片,應用全細胞膜片鉗技術(shù)記錄SG神經(jīng)元的電生理學特點及接受超極化刺激后的反應,并觀察超極化激活環(huán)核苷酸門控陽離子(HCN)通道阻斷劑和T型鈣(Cav3)通道阻斷劑對去極化反跳的作用。結(jié)果共記錄了63個SG神經(jīng)元的電活動,其中23個無去極化反跳,19個為去極化反跳無放電,21個為去極化反跳伴放電。無去極化反跳組SG神經(jīng)元的動作電位閾值(-28.7±1.6 m V)明顯高于去極化反跳伴放電組(-36.0±2.0 m V)(P0.05)。HCN通道阻斷劑氯化銫和ZD7288可顯著延長去極化反跳伴放電的潛伏期,分別從45.9±11.6 ms增加到121.6±51.3 ms(P0.05)和從36.2±10.3 ms增加到73.6±13.6 ms(P0.05);ZD7288也能顯著延長去極化反跳不伴放電的潛伏期,從71.9±35.1 ms增加到267.0±68.8 ms(P0.05),而T型鈣通道阻斷劑氯化鎳和米貝地爾可顯著降低去極化反跳伴放電的振幅,分別從19.9±6.3 m V降到9.5±4.5 m V(P0.05)和從26.1±9.4 m V降到15.5±5.0 m V(P0.05),米貝地爾同樣能顯著降低去極化反跳不伴放電的振幅,從14.3±3.0 m V降低至7.9±2.0 m V(P0.05)。結(jié)論近2/3的SG神經(jīng)元有去極化反跳,其潛伏期和振幅分別受HCN通道和T型鈣通道調(diào)控。
[Abstract]:Objective to study the mechanism of depolarization rebound and regulation of (SG) neurons in dorsal horn of spinal cord in order to provide reference for clinical treatment of depolarization rebound related diseases. Methods Longitudinal sections of the spinal cord were made from 3 to 5 week old SD rats. The electrophysiological characteristics of SG neurons and the response to hyperpolarization were recorded by whole-cell patch clamp technique. The effects of hyperpolarization-activated cyclic nucleotide-gated cationic (HCN) channel blockers and T-type calcium (Cav3) channel blockers on depolarization rebound were observed. Results the electrical activity of 63 SG neurons was recorded, including 23 without depolarization, 19 without depolarization and 21 with depolarization. The action potential threshold (-28.7 鹵1.6 m V) of SG neurons in the non-depolarized backjumper group was significantly higher than that in the depolarized rebound group (-36.0 鹵2.0 m V) (, P0.05). Cesium chloride and ZD7288, a). HCN channel blocker, were significantly higher than those in the depolarization rebound group (-36.0 鹵2.0 m V) (). Prolonging the latency of depolarization rebound accompanied by discharge, It increased from 45.9 鹵11.6 ms to 121.6 鹵51.3 ms (P0.05) and from 36.2 鹵10.3 ms to 73.6 鹵13.6 ms (P0.05). ZD7288 also significantly prolonged the latency of depolarization rebound without discharges, from 71.9 鹵35.1 ms to 267.0 鹵68.8 ms (P0.05), while the T-type calcium channel blockers, nickel chloride and mebedil, significantly decreased the amplitude of depolarization rebound accompanied discharges. From 19.9 鹵6.3 MV to 9.5 鹵4.5 m V (P0.05) and from 26.1 鹵9.4 MV to 15.5 鹵5.0 m V (P0.05), mibedil also significantly decreased the amplitude of depolarization rebound without discharges. It decreased from 14.3 鹵3.0 MV to 7.9 鹵2.0 m V (P0.05). Conclusion nearly 2 / 3 of SG neurons have depolarization rebound, their latency and amplitude are regulated by HCN channel and T type calcium channel respectively.
【作者單位】： 南昌大學第一附屬醫(yī)院疼痛科;南昌大學第一附屬醫(yī)院兒科;深圳市南山醫(yī)院韓濟生院士疼痛醫(yī)學工作站;南昌大學第一附屬醫(yī)院醫(yī)學科研中心;
【基金】：國家自然科學基金(81560198,31660289) 南昌大學研究生創(chuàng)新基金(cx2015166)~~
【分類號】：R338

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