神经病理性疼痛
坏死性下垂
多巴胺
神经炎症
被盖腹侧区
痛觉过敏
神经科学
医学
伤害
药理学
炎症
化学
内科学
生物
程序性细胞死亡
多巴胺能
受体
细胞凋亡
生物化学
作者
Jun Wang,Nan Zhang,Hong-Zheng Liu,Jinliang Wang,Yongbo Zhang,Dongdong Su,Limin Zhang,Baodong Li,Hui‐Tao Miao,Jun Miao
标识
DOI:10.1016/j.brainresbull.2024.111168
摘要
Neuropathic pain (NP) constitutes a significant burden for individuals, manifesting as nociceptive anaphylaxis, hypersensitivity, and spontaneous pain. Previous research has suggested that the analgesic effects of NP are mediated by dopamine (DA) neurons in the ventral tegmental region (VTA) through projections to various brain regions. A decrease in VTA dopamine neurons following NP may contribute to prolonged pain. It has been revealed that inflammatory activation triggers necroptosis by stimulating mixed lineage kinase domain-like protein (MLKL), leading to progressive neuronal demise. Recent research from many studies has revealed that that IL-17-induced necroptosis plays an important role in neuroinflammation and neuronal damage. To our knowledge, few studies have hitherto investigated how IL-17-induced necroptosis may contribute to neuropathic pain. Hydrogen sulfide (H
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