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中国临床药理学与治疗学 ›› 2017, Vol. 22 ›› Issue (9): 1008-1011.

• 基础研究 • 上一篇    下一篇

NR2A拮抗剂对神经病理性痛大鼠海马突触长时程增强的影响

魏辉明,麻伟青,李文锋,王慧明   

  1. 解放军昆明总医院麻醉科,昆明650032,云南
  • 收稿日期:2017-06-16 修回日期:2017-07-21 出版日期:2017-09-26 发布日期:2017-09-30
  • 通讯作者: 麻伟青,女,硕士,主任医师,研究方向:麻醉及疼痛药理学。 Tel: 0871-4774725 E-mail: ma_weiqing@163.com
  • 作者简介:魏辉明,男,博士,主任医师,研究方向:麻醉及疼痛药理学。 Tel: 0871-4774724   E-mail: medicana@sina.com
  • 基金资助:

    成都军区“十二五”医学科研项目(B14013)

Effect of antagonist of NR2A-containing N-methyl-D-aspartate receptors on synaptic long-term potentiation in hippocampus in rats with neuropathic pain

WEI Huiming, MA Weiqing, LI Wenfeng, WANG Huiming   

  1. Department of Anesthesiology, Kunming General Hospital of PLA, Kunming 650032, Yunnan, China
  • Received:2017-06-16 Revised:2017-07-21 Online:2017-09-26 Published:2017-09-30

摘要:

目的: 探讨含2A亚基的N-甲基-D-门冬氨酸(NMDA)受体(NR2A)拮抗剂NVP-AAM077对神经病理性痛大鼠海马突触长时程增强(LTP)的影响。方法: 24只成年雄性Wistar大鼠随机分为4组(n=6):假手术组(S组)、S+NVP-AAM077组(SN组)、神经病理性痛模型组(NP组)、NP+NVP-AAM077组(NPN组)。采用结扎L4和L5右侧脊神经的方法制备大鼠神经病理性痛模型;记录海马CA1区兴奋性突触后电位(EPSP),以高频刺激(HFS)诱发LTP。SN组和NPN组给予HFS前20 min经侧脑室输注NVP-AAM077 (NR2A特异性阻断剂) 5 μL(1.5 μg)。结果: 与S组和SN组比较,NP组和NPN组各时点痛阈降低;NP组和NPN组EPSP幅值升高(P<0.05),NP组与NPN组差异无统计学意义。结论: NR2A与神经病理性痛大鼠海马突触LTP的易化作用关系不大。

关键词: 神经痛, 长时程增强, N-甲基-D-门冬氨酸受体, 海马

Abstract:

AIM: To investigate the effect of antagonist of NR2A-containing N-methyl-D-aspartate (NMDA) receptors on synaptic long-term potentiation (LTP) in the hippocampus in rats with neuropathic pain. METHODS: Twenty-four adult male Wistar rats were randomly divided into four groups (n=6 each ): sham operating group (group S), S+NVP-AAM077 group (group SN), neuropathic pain group (group NP) and NP+NVP-AAM077 group (group NPN). Neuropathic pain was produced by ligation of the right L4 and L5 spinal nerve. The excitatory post-synaptic potential (EPSP) in hippocampal CA1 region was measured at 3 day after the last measurement of pain threshold. The changes in EPSP and LTP of the CA1 stratum radiatum of the rat hippocampus were observed using stereotaxic technology and extracellular recording respectively. RESULTS: The pain threshold was significantly lower in group NP and NPN, and the amplitude of EPSP was significantly higher in group NP and NPN than in group S and SN (P<0.05), but there was no significant difference in the amplitude of EPSP between group NP and NPN. CONCLUSION: The facilitation of LTP induction by neuropathic pain in the CA1 area of the hippocampus may be little relationship with the activation of NR2A-containing NMDA receptors.

Key words: neuralgia, long-term potentiation, N-methyl-D-aspartate receptors, hippocampus

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