慢性应激诱导慢性痛-抑郁共病机制研究进展
Research Progress on the Mechanism of Chronic Stress-Induced Comorbidity between Chronic Pain and Depression
侯锦雯 1邢国刚1
作者信息
- 1. 北京大学神经科学研究所,北京大学基础医学院神经生物学系,教育部/卫健委神经科学重点实验室,北京 100191
- 折叠
摘要
慢性疼痛(简称慢性痛)和抑郁障碍是危害人类健康的两类常见疾病.慢性痛和抑郁常常伴随发生,相互影响,极大地提高了治疗难度.慢性痛和抑郁的发生具有共同或相互作用的神经回路及神经递质系统,神经炎症在慢性痛和抑郁的发病中也都具有重要作用.相关神经回路功能障碍和神经炎症是慢性痛-抑郁共病的重要机制.慢性应激(chronic stress)是诱发抑郁和慢性痛的重要原因.以往的研究表明,下丘脑-垂体-肾上腺(hypothalamic-pituitary-adrenal,HPA)轴功能紊乱是慢性应激诱导抑郁及共病疼痛的病理基础,慢性应激可能通过HPA轴功能紊乱,促进神经炎症反应和神经回路功能障碍,导致慢性痛-抑郁共病.本文就慢性应激诱导慢性痛-抑郁共病的发病机制进行探讨,从HPA轴功能、神经炎症、涉及的大脑结构和神经回路等方面阐述慢性应激诱导慢性痛-抑郁共病的发病机制.
Abstract
Chronic pain and depression are two common diseases that endanger human health.They often co-occur and mutually influence each other,greatly increasing the difficulty of treat-ment.The occurrence of chronic pain and depression involves common or interacting neural cir-cuits and neurotransmitter systems.Neuroinflammation also plays an important role in the path-ogenesis of chronic pain and depression.Dysfunction in related neural circuitry and neuroinflam-mation are important mechanisms underlying the comorbidity between chronic pain and depres-sion.Chronic stress is a critical cause of inducing depression and chronic pain.Previous studies have shown that dysfunction of the hypothalamic-pituitary-adrenal(HPA)axis is the pathological basis for chronic stress-induced depression and comorbid pain.Chronic stress may promote neu-roinflammatory response and dysfunction of neural circuits through HPA axis dysfunction,lead-ing to the comorbidity of chronic pain and depression.This review discusses the pathogenesis of chronic stress-induced pain comorbid with depression,and elaborates on the pathogenesis of chro-nic stress-induced comorbidity of chronic pain and depression from the aspects of the HPA axis function,neuroinflammation,brain structure and neural circuits involved.
关键词
慢性应激/慢性痛-抑郁共病/HPA轴/神经炎症/神经环路Key words
chronic stress/chronic pain-depression comorbid/HPA axis/neuroinflammation/neural circuit引用本文复制引用
基金项目
国家自然科学基金(82371227)
国家自然科学基金(82171226)
国家自然科学基金(81974169)
北京市自然科学基金(7222105)
出版年
2024
NETL
NSTL
万方数据