南方医科大学学报

南方医科大学学报 ›› 2017, Vol. 37 ›› Issue (02): 204-.

• • 上一篇    下一篇

大鼠脊髓背角胶状质神经元的去极化反跳及调控机制

李凌超，张达颖，彭斯聪，吴静，蒋昌宇，柳涛   

  • 出版日期:2017-02-20 发布日期:2017-02-20

Rebound depolarization of substantia gelatinosa neurons and its modulatory mechanisms in rat spinal dorsal horn

  • Online:2017-02-20 Published:2017-02-20

HTML

PDF

1651

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 mV）明显高于去极化反跳伴放电组（-36.0±2.0 mV）（P<0.05）。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（P<0.05）和从 36.2±10.3 ms 增加到73.6±13.6 ms（P<0.05）；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（P<0.05），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 mV降 到9.5±4.5 mV（P<0.05）和从26.1±9.4 mV降到15.5±5.0 mV（P<0.05），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 mV降低至7.9±2.0 mV（P<0.05）。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 investigate the rebound depolarization of substantia gelatinosa (SG) neurons in rat spinal dorsal horn and explore its modulatory mechanisms to provide better insights into rebound depolarization-related diseases. Methods Parasagittal slices of the spinal cord were prepared from 3- to 5-week-old Sprague-Dawley rats. The electrophysiologic characteristics and responses to hyperpolarization stimulation were recorded using whole-cell patch-clamp technique. The effects of hyperpolarization-activated cyclic nucleotide gated cation (HCN) channel blockers and T-type calcium channel blockers on rebound depolarization of the neurons were studied. Results A total of 63 SG neurons were recorded. Among them, 23 neurons showed no rebound depolarization, 19 neurons showed rebound depolarization without spikes, and 21 neurons showed rebound depolarization with spikes. The action potential thresholds of the neurons without rebound depolarization were significantly higher than those of the neurons with rebound depolarization and spikes (-28.7 ± 1.6 mV vs -36.0 ± 2.0 mV, P<0.05). The two HCN channel blockers CsCl and ZD7288 significantly delayed the latency of rebound depolarization with spike from 45.9 ± 11.6 ms to 121.6 ± 51.3 ms (P<0.05) and from 36.2 ± 10.3 ms to 73.6 ± 13.6 ms (P<0.05), respectively. ZD7288 also significantly prolonged the latency of rebound depolarization without spike from 71.9±35.1 ms to 267.0 ± 68.8 ms (P<0.05). The T-type calcium channel blockers NiCl2 and mibefradil strongly decreased the amplitude of rebound depolarization with spike from 19.9 ± 6.3 mV to 9.5±4.5 mV (P<0.05) and from 26.1±9.4 mV to 15.5±5.0 mV (P<0.05), respectively. Mibefradil also significantly decreased the amplitude of rebound depolarization without spike from 14.3 ± 3.0 mV to 7.9 ± 2.0 mV (P<0.05). Conclusion Nearly two-thirds of the SG neurons have rebound depolarizations modulated by HCN channel and T-type calcium channel.