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作 者:李建民[1] 昝志[1] 宫圆圆[1] 刘洁[1] 刘暾[1] 吕岩[1]
机构地区:[1]第四军医大学西京医院麻醉科,西安710032
出 处:《神经解剖学杂志》2014年第2期135-140,共6页Chinese Journal of Neuroanatomy
基 金:国家自然科学基金(31070977)
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CB1受体,NADA可以显著抑制由Aδ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Aδ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。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.
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