Neuroscience Program, Department of Physiology, Michigan State University, East Lansing, Michigan.
Neuroscience Program, Department of Physiology, Michigan State University, East Lansing, Michigan.
Cell Mol Gastroenterol Hepatol. 2019;7(2):433-445. doi: 10.1016/j.jcmgh.2018.11.005. Epub 2018 Nov 24.
Chronic abdominal pain is the most common gastrointestinal issue and contributes to the pathophysiology of functional bowel disorders and inflammatory bowel disease. Current theories suggest that neuronal plasticity and broad alterations along the brain-gut axis contribute to the development of chronic abdominal pain, but the specific mechanisms involved in chronic abdominal pain remain incompletely understood. Accumulating evidence implicates glial cells in the development and maintenance of chronic pain. Astrocytes and microglia in the central nervous system and satellite glia in dorsal root ganglia contribute to chronic pain states through reactive gliosis, the modification of glial networks, and the synthesis and release of neuromodulators. In addition, new data suggest that enteric glia, a unique type of peripheral glia found within the enteric nervous system, have the potential to modify visceral perception through interactions with neurons and immune cells. Understanding these emerging roles of enteric glia is important to fully understand the mechanisms that drive chronic pain and to identify novel therapeutic targets. In this review, we discuss enteric glial cell signaling mechanisms that have the potential to influence chronic abdominal pain.
慢性腹痛是最常见的胃肠道问题，也是功能性肠病和炎症性肠病病理生理学的基础。目前的理论表明，神经元可塑性和沿脑-肠轴的广泛改变有助于慢性腹痛的发展，但涉及慢性腹痛的具体机制仍不完全清楚。越来越多的证据表明神经胶质细胞参与了慢性疼痛的发展和维持。中枢神经系统中的星形胶质细胞和小胶质细胞以及背根神经节中的卫星胶质细胞通过反应性神经胶质增生、胶质网络的改变以及神经调质的合成和释放，导致慢性疼痛状态。此外，新的数据表明，肠神经胶质细胞，一种存在于肠神经系统内的独特的外周神经胶质细胞，有可能通过与神经元和免疫细胞的相互作用来改变内脏感觉。了解肠神经胶质细胞的这些新作用对于全面了解驱动慢性疼痛的机制和确定新的治疗靶点非常重要。在这篇综述中，我们讨论了有可能影响慢性腹痛的肠神经胶质细胞信号转导机制。
