神经科学
神经病理性疼痛
下调和上调
胶质纤维酸性蛋白
炎症
神经系统
感觉系统
神经损伤
慢性疼痛
神经元
感觉神经元
医学
痛觉过敏
小胶质细胞
生物
伤害
病理
免疫学
受体
内科学
免疫组织化学
基因
生物化学
作者
Menachem Hanani,David C. Spray
标识
DOI:10.1038/s41583-020-0333-z
摘要
Satellite glial cells (SGCs) closely envelop cell bodies of neurons in sensory, sympathetic and parasympathetic ganglia. This unique organization is not found elsewhere in the nervous system. SGCs in sensory ganglia are activated by numerous types of nerve injury and inflammation. The activation includes upregulation of glial fibrillary acidic protein, stronger gap junction-mediated SGC-SGC and neuron-SGC coupling, increased sensitivity to ATP, downregulation of Kir4.1 potassium channels and increased cytokine synthesis and release. There is evidence that these changes in SGCs contribute to chronic pain by augmenting neuronal activity and that these changes are consistent in various rodent pain models and likely also in human pain. Therefore, understanding these changes and the resulting abnormal interactions of SGCs with sensory neurons could provide a mechanistic approach that might be exploited therapeutically in alleviation and prevention of pain. We describe how SGCs are altered in rodent models of four common types of pain: systemic inflammation (sickness behaviour), post-surgical pain, diabetic neuropathic pain and post-herpetic pain.
科研通智能强力驱动
Strongly Powered by AbleSci AI