大鼠脊髓背角胶状质神经元的去极化反跳及调控机制
发布时间：2019-01-04 17:59
【摘要】：目的研究大鼠脊髓背角胶状质(SG)神经元的去极化反跳及调控机制,以期对去极化反跳相关疾病的临床治疗提供参考。方法选取3~5周龄SD大鼠,制作离体脊髓纵切片,应用全细胞膜片钳技术记录SG神经元的电生理学特点及接受超极化刺激后的反应,并观察超极化激活环核苷酸门控阳离子(HCN)通道阻断剂和T型钙(Cav3)通道阻断剂对去极化反跳的作用。结果共记录了63个SG神经元的电活动,其中23个无去极化反跳,19个为去极化反跳无放电,21个为去极化反跳伴放电。无去极化反跳组SG神经元的动作电位阈值(-28.7±1.6 m V)明显高于去极化反跳伴放电组(-36.0±2.0 m V)(P0.05)。HCN通道阻断剂氯化铯和ZD7288可显著延长去极化反跳伴放电的潜伏期,分别从45.9±11.6 ms增加到121.6±51.3 ms(P0.05)和从36.2±10.3 ms增加到73.6±13.6 ms(P0.05);ZD7288也能显著延长去极化反跳不伴放电的潜伏期,从71.9±35.1 ms增加到267.0±68.8 ms(P0.05),而T型钙通道阻断剂氯化镍和米贝地尔可显著降低去极化反跳伴放电的振幅,分别从19.9±6.3 m V降到9.5±4.5 m V(P0.05)和从26.1±9.4 m V降到15.5±5.0 m V(P0.05),米贝地尔同样能显著降低去极化反跳不伴放电的振幅,从14.3±3.0 m V降低至7.9±2.0 m V(P0.05)。结论近2/3的SG神经元有去极化反跳,其潜伏期和振幅分别受HCN通道和T型钙通道调控。
[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 卤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 卤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 卤2.0 m V) (). Prolonging the latency of depolarization rebound accompanied by discharge, It increased from 45.9 卤11.6 ms to 121.6 卤51.3 ms (P0.05) and from 36.2 卤10.3 ms to 73.6 卤13.6 ms (P0.05). ZD7288 also significantly prolonged the latency of depolarization rebound without discharges, from 71.9 卤35.1 ms to 267.0 卤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 卤6.3 MV to 9.5 卤4.5 m V (P0.05) and from 26.1 卤9.4 MV to 15.5 卤5.0 m V (P0.05), mibedil also significantly decreased the amplitude of depolarization rebound without discharges. It decreased from 14.3 卤3.0 MV to 7.9 卤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.
【作者单位】： 南昌大学第一附属医院疼痛科;南昌大学第一附属医院儿科;深圳市南山医院韩济生院士疼痛医学工作站;南昌大学第一附属医院医学科研中心;
【基金】：国家自然科学基金(81560198,31660289) 南昌大学研究生创新基金(cx2015166)~~
【分类号】：R338
[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 卤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 卤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 卤2.0 m V) (). Prolonging the latency of depolarization rebound accompanied by discharge, It increased from 45.9 卤11.6 ms to 121.6 卤51.3 ms (P0.05) and from 36.2 卤10.3 ms to 73.6 卤13.6 ms (P0.05). ZD7288 also significantly prolonged the latency of depolarization rebound without discharges, from 71.9 卤35.1 ms to 267.0 卤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 卤6.3 MV to 9.5 卤4.5 m V (P0.05) and from 26.1 卤9.4 MV to 15.5 卤5.0 m V (P0.05), mibedil also significantly decreased the amplitude of depolarization rebound without discharges. It decreased from 14.3 卤3.0 MV to 7.9 卤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.
【作者单位】： 南昌大学第一附属医院疼痛科;南昌大学第一附属医院儿科;深圳市南山医院韩济生院士疼痛医学工作站;南昌大学第一附属医院医学科研中心;
【基金】：国家自然科学基金(81560198,31660289) 南昌大学研究生创新基金(cx2015166)~~
【分类号】：R338
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