中文摘要：

目的：探讨内源性大麻素配体NADA对脊髓背角II层胶状质（sG）神经元突触兴奋性的影响及其在神经病理性痛模型上的镇痛作用。方法：利用膜片钳技术，观察NADA（40μmol／L）对sG神经元自发性兴奋性突触后电流（sEPSC）及背根诱发兴奋性突触后电流（eEPSC）的影响。制备脊神经结扎（SNL）模型，观察鞘内注射20μgNADA对机械性缩足反射阈值（PWMT）的影响。结果：通过作用于CBl受体，NADA可以显著抑制由A8纤维及C纤维介导单突触eEPSC的幅值，并且显著减低sEPSC频率而对其幅度无改变。在神经病理性痛模型中，与对照侧相比，NADA可以显著增加手术侧机械缩足反射阈值（P〈0．0001），而溶剂组则无统计学意义（P〉0．05）。结论：内源性大麻素配体NADA能够抑制脊髓背角浅层A8纤维及C纤维介导的突触传递，并且可以减轻实验动物的神经病理性疼痛。

英文摘要：

Objective： To determine the effects of NADA on excitatory synaptic transmission of SG neurons and its effect on allodynia in a neuropathic pain animal model. Methods： Adult Sprague-Dawley rats （4-6 weeks old） were anaesthetized to make spinal cord slices. Whole-cell, voltage-clamp recordings were done in SG neurons to investigate the effect of NADA （40 p, mol/L） on spontaneous EPSC （sEPSC） and dorsal root evoked EPSC （eEPSC）. Sprague-Dawley rats were used to made SNL neuropathic pain model, paw withdrawal mechanical threshold （PWMT） was measured after intrathecal injection of 20 μg NADA. Results： NADA significantly inhibited the peak amplitude of monosynaptic eEPSC of A8 and C fibers via CB1 receptor, decreased the frequency of sEPSC without affecting its amplitude. NADA significantly increased PWMT （P 〈 O. 0001 ） when compares with the control side, while vehicle group had no statistical significance （P 〉 0.05）. Conclusion： Endocannabinoid NADA night alleviate neuropathic pain in experimental animals through inhibition excitatory synaptic transmission of SG neurons in the spinal dorsal horn.