Department of Anatomy, School of Medical Sciences, Faculty of Medicine University of New South Wales, Sydney, New South Wales, Australia.
J Neurosci Res. 2012 Feb;90(2):337-45. doi: 10.1002/jnr.22764. Epub 2011 Oct 4.
Gap junctions are specialized transmembrane channels that allow rapid electrical signalling and direct intercellular communication for maintenance and coordination of normal cellular activities and homeostasis. Although gap junction channels in the nervous system mediate intercellular coupling between glial cells and between neurons, they also contribute to the spread of secondary damage and inflammation under pathological conditions. There is now evidence of the involvement of gap junctions in chronic pain caused by nervous system damage or tissue inflammation. In this Mini-Review, we highlight recent studies demonstrating the dynamic plasticity of gap junctions in response to nervous system injury and the effects of gap junction blockade on neuronal survival and modulation of pain in animal models of neuropathic and inflammatory pain. The involvement of dorsal root ganglia and spinal cord gap junctions in mediating chronic pain and the potential for targeting connexins as a novel modality for the treatment of intractable pain syndromes arising from nervous system injury and disorders are discussed.
缝隙连接是一种特殊的跨膜通道，允许快速的电信号传递和直接的细胞间通讯，以维持和协调正常细胞活动和内稳态。尽管神经系统中的缝隙连接通道介导神经胶质细胞之间和神经元之间的细胞间偶联，但它们也有助于在病理条件下继发性损伤和炎症的扩散。现在有证据表明，缝隙连接参与了由神经系统损伤或组织炎症引起的慢性疼痛。在这篇迷你综述中，我们强调了最近的研究，这些研究表明缝隙连接在神经系统损伤时的动态可塑性，以及缝隙连接阻断对神经元存活和动物模型中神经性和炎症性疼痛调制的影响。讨论了背根神经节和脊髓缝隙连接在介导慢性疼痛中的作用，以及将连接蛋白作为一种治疗由神经系统损伤和疾病引起的难治性疼痛综合征的新方法的潜力。
