Department of Anesthesiology, Shanghai Children's Medical Center, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Department of Anesthesiology and Intensive Care Medicine, Xinhua Hospital, College of Medicine, Shanghai Jiaotong University, Shanghai, China.
Sci Rep. 2018 Jan 26;8(1):1691. doi: 10.1038/s41598-018-20080-2.
The pathophysiology of neuropathic pain generation has not been fully investigated. Previous studies have primarily focused on changes in the properties of single neurons in the brain after nerve injury; however, little is known concerning the role of neuron-to-neuron connections in neuropathic pain pathogenesis. Synaptic transmission potentiation in anterior cingulate cortex (ACC) has been confirmed to be responsible for the formation of neuropathic pain. Thus, analysis of interneuronal connections in the ACC is an important approach for understanding the mechanism of neuropathic pain since it provides information on the potency of synaptic transmission. Here, we recorded membrane potentials from pairs of ACC neurons in anaesthetised rats and found that cross-correlations between pairs of ACC neurons significantly increased after surgery for chronic constriction injury (CCI). Moreover, CCI surgery could also enhance the power spectrum density of lower and higher-frequency membrane oscillations while having no effect on middle-frequency oscillations. The activation of membrane potential synchrony and power spectrum was reversed by the electrical synapse blocker mefloquine and pain behaviour was simultaneously alleviated. Our results may indicate that activation of membrane potential synchrony contributes to generation of neuropathic pain.
神经病理性疼痛产生的病理生理学尚未得到充分研究。先前的研究主要集中在神经损伤后大脑中单神经元特性的变化上;然而,对于神经元之间连接在神经病理性疼痛发病机制中的作用知之甚少。已证实扣带前皮质 (ACC) 中的突触传递增强是导致神经病理性疼痛形成的原因。因此,分析 ACC 中的中间神经元连接是理解神经病理性疼痛机制的重要方法,因为它提供了关于突触传递强度的信息。在这里,我们记录了麻醉大鼠 ACC 神经元对的膜电位,并发现慢性缩窄性损伤 (CCI) 手术后,ACC 神经元对之间的互相关显著增加。此外,CCI 手术还可以增强低频和高频膜振荡的功率谱密度,而对中频振荡没有影响。膜电位同步和功率谱的激活被电突触阻滞剂甲氟喹逆转,同时疼痛行为也得到缓解。我们的结果可能表明,膜电位同步的激活有助于神经病理性疼痛的产生。