Adverse effects of early-life stress:focus on the rodent neuroendocrine system
作者机构:Department of Molecular BiologyCollege of Natural SciencesPusan National UniversityBusanRepublic of Korea
出 版 物:《Neural Regeneration Research》 (中国神经再生研究(英文版))
年 卷 期:2024年第19卷第2期
页 面:336-341页
核心收录:
学科分类:0710[理学-生物学] 07[理学] 071006[理学-神经生物学]
基 金:supported by the National Research Foundation of Korea(NRF)grant funded by the Korea government(MSIT)(No.2021R1C1C100328611) Pusan National University Research Grant,2020(both to EMJ)
主 题:early-life stress hypothalamic-pituitary-adrenergic axis maternal separation mental illness neurodevelopmental disorder neuroendocrine system neurotransmitter
摘 要:Early-life stress is associated with a high prevalence of mental illnesses such as post-traumatic stress disorders,attention-deficit/hyperactivity disorder,schizophrenia,and anxiety or depressive behavior,which constitute major public health *** the early stages of brain development after birth,events such as synaptogenesis,neuron maturation,and glial differentiation occur in a highly orchestrated manner,and external stress can cause adverse long-term effects throughout *** body utilizes multifaceted mechanisms,including neuroendocrine and neurotransmitter signaling pathways,to appropriately process external *** individuals first exposed to early-life stress deploy neurogenesis as a stress-defense mechanism;however,in adulthood,early-life stress induces apoptosis of mature neurons,activation of immune responses,and reduction of neurotrophic factors,leading to anxiety,depression,and cognitive and memory *** process involves the hypothalamus-pituitary-adrenal axis and neurotransmitters secreted by the central nervous system,including norepinephrine,dopamine,and *** rodent early-life stress model is generally used to experimentally assess the effects of stress during *** paper reviews the use of the early-life stress model and stress response mechanisms of the body and discusses the experimental results regarding how early-life stress mediates stress-related pathways at a high vulnerability of psychiatric disorder in adulthood.