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作 者:侯锦雯 邢国刚[1] HOU Jin-Wen;XING Guo-Gang(Neuroscience Research Institute,Peking University,Department of Neurobiology,School of Basic Medical Sciences,Peking University Health Science Center,Key Laboratory for Neuroscience,Ministry of Education of China&National Health Commission of China,Beijing 100191,China)
机构地区:[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
出 处:《生理科学进展》2024年第3期191-198,共8页Progress in Physiological Sciences
基 金:国家自然科学基金(82371227,82171226,81974169);北京市自然科学基金(7222105)资助课题。
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。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 treatment.The occurrence of chronic pain and depression involves common or interacting neural circuits and neurotransmitter systems.Neuroinflammation also plays an important role in the pathogenesis of chronic pain and depression.Dysfunction in related neural circuitry and neuroinflammation are important mechanisms underlying the comorbidity between chronic pain and depression.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 neuroinflammatory response and dysfunction of neural circuits through HPA axis dysfunction,leading 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 chronic stress-induced comorbidity of chronic pain and depression from the aspects of the HPA axis function,neuroinflammation,brain structure and neural circuits involved.
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