[大鼠脊髓背角胶状质神经元的反弹去极化及其调节机制]
[Rebound depolarization of substantia gelatinosa neurons and its modulatory mechanisms in rat spinal dorsal horn].
作者信息
Li Ling-Chao, Zhang Da-Ying, Peng Si-Cong, Wu Jing, Jiang Chang-Yu, Liu Tao
机构信息
Department of Pain Clinic, First Affiliated Hospital of Nanchang University, Nanchang, 330006, China. E-mail:
出版信息
Nan Fang Yi Ke Da Xue Xue Bao. 2016 Feb 20;37(2):204-209. doi: 10.3969/j.issn.1673-4254.2017.02.10.
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.
目的
研究大鼠脊髓背角胶状质（SG）神经元的反弹去极化现象，并探讨其调节机制，以便更好地了解与反弹去极化相关的疾病。
方法
从3至5周龄的Sprague-Dawley大鼠制备脊髓矢状切片。采用全细胞膜片钳技术记录电生理特征和对超极化刺激的反应。研究超极化激活的环核苷酸门控阳离子（HCN）通道阻滞剂和T型钙通道阻滞剂对神经元反弹去极化的影响。
结果
共记录63个SG神经元。其中，23个神经元未表现出反弹去极化，19个神经元表现出无锋电位的反弹去极化，21个神经元表现出有锋电位的反弹去极化。无反弹去极化的神经元的动作电位阈值显著高于有反弹去极化和锋电位的神经元（-28.7±1.6 mV对-36.0±2.0 mV，P<0.05）。两种HCN通道阻滞剂氯化铯和ZD7288分别使有锋电位的反弹去极化潜伏期从45.9±11.6 ms显著延长至121.6±51.3 ms（P<0.05）和从36.2±10.3 ms显著延长至73.6±13.6 ms（P<0.05）。ZD7288还使无锋电位的反弹去极化潜伏期从71.9±35.1 ms显著延长至267.0±68.8 ms（P<0.05）。T型钙通道阻滞剂氯化镍和米贝地尔分别使有锋电位的反弹去极化幅度从19.9±6.3 mV显著降低至9.5±4.5 mV（P<0.05）和从26.1±9.4 mV显著降低至15.5±5.0 mV（P<0.05）。米贝地尔还使无锋电位的反弹去极化幅度从14.3±3.0 mV显著降低至7.9±2.0 mV（P<0.05）。
结论
近三分之二的SG神经元具有受HCN通道和T型钙通道调节的反弹去极化。
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