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不同神经病理性疼痛模型下钠通道αⅢmRNA表达的改变 被引量:2

Changes of αⅢ sodium channel expression in dorsal root ganglion in the different models of chronic neuropathic pain
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摘要 目的观察大鼠背根神经节(DRG)电压门控钠通道αⅢ在不同疼痛模型中的变化,探讨慢性神经痛的发生机制。方法SD大鼠18只,随机均分为三组:坐骨神经慢性压迫性损伤组(CCI组),保留性神经损伤组(SNI组),假手术组。实验动物采用组内同侧与对侧自体对照以及组间比较,于术前2d和术后1、3、5、7、9、11、13d测定机械痛阈和热痛阈,术后14d取大鼠双侧L4、L5和L6DRG,以逆转录聚合酶链反应(RT-PCR)半定量分析CCI与SNI模型大鼠相应DRG钠通道αⅢ转录物的变化。结果CCI组大鼠损伤侧于术后5d出现热痛觉过敏和触诱发痛(P<0·05),术后13d痛敏达到高峰(P<0·01),并发现感觉神经元特异性的TTX-S钠通道转录物αⅢ出现明显表达,而健侧和假手术组没有表达;SNI组大鼠术后1d即出现明显触诱发痛,13d触诱发痛达到高峰(P<0·01),但热痛觉过敏不明显,和假手术组相似,双侧的αⅢ均未表达。结论CCI模型大鼠术后热痛觉过敏较为明显,而SNI模型大鼠术后出现明显触诱发痛;慢性神经痛模型损伤侧初级感觉神经元过度兴奋与钠通道表达异常有关,但不同的神经痛模型其αⅢ表达结果不同,提示钠通道表达存在不同的影响机制。 Objective To investigate the changes of αⅢ sodium channel transcript in dorsal root ganglion(DRG) neurons in different models of chronic neuropathic pain.Methods Eighteen rats were divided into 3 groups with 6 animals each.The CCI model was made by loose ligation of sciatic nerve by chronic and the SNI model was established by tight ligation and section of tiblal and the common peroneal nerve and leaving the sural nerve intact.The mechanical and thermal pain threshold were measured before operation and on the 1st,3rd,5th,7th,9th,11th and 13th postoperative day.The animals were deeply anesthetized and rapidly decapitated on the 14th day after surgery.The L_4,L_5 and L_6 DRG of the operated side was removed and crushed and total RNA was extracted with trizol reagent.The contralateral side was used as control.The change of αⅢsodium channel expression was determined by semi-reverse transcriptase-PCR.Results Pain threshold was significantly lowered after CCI and SNI as compared with that in control group.Sensory neuron specific TTX-S sodium channel αⅢ transcript was elevated after CCI as compared with that in control group(no expression was detected).In contrast,there was no marked change of αⅢsodium channel transcript in dorsal root ganglion(DRG)neurons in SNI model.Conclusion In CCI group,the rats developed obvious thermal hyperalgesia after operation,while in SNI group they mainly exhibited mechanical allodynia.Sodium channel αⅢ is involved in the hyperexcitability of the primary sensory neurons after CCI but not in SNI model. [
出处 《临床麻醉学杂志》 CAS CSCD 2005年第5期344-346,共3页 Journal of Clinical Anesthesiology
关键词 神经病理性疼痛 钠通道 αⅢmRNA表达 DRG 疼痛模型 Neuropathic pain αⅢsodium channel Animal model
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参考文献13

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同被引文献27

  • 1金小高,罗爱林,王金韬,张广雄,万丽,安珂,徐颖,田玉科.脊髓神经元和胶质细胞激活在三种神经病理性疼痛大鼠模型脊髓水平致痛机制中的作用[J].中华麻醉学杂志,2006,26(1):71-74. 被引量:11
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