University of South Carolina School of Medicine, Department of Pharmacology, Physiology and Neuroscience.
Curr Neuropharmacol. 2014 Mar;12(2):205-11. doi: 10.2174/1570159X11666131120224413.
Stress initiates a cascade of complex neural and peripheral changes that promote healthy adaption to stress, but when unabated, leads to pathology. Fascinating individual differences arise in the ability to cope with a stressor, rendering an individual more or less likely to develop stress-induced pathologies such as depression, anxiety, and cardiovascular disease. In this review we evaluate recent findings that investigate the neural underpinnings of adopting a passive or active coping response during social defeat stress. Because passive coping is associated with vulnerability to stress-related pathologies and active coping confers resiliency, understanding neurobiological adaptations associated with these diverse coping strategies may reveal biomarkers or targets impacting stress susceptibility. The co-occurrence of stress-induced depression and cardiovascular disease is becoming increasingly clear. Therefore this review focuses on the central mechanisms capable of contributing to psychopathology and cardiovascular disease such as corticotropin releasing factor, neuropeptide Y, monoamines, cytokines and oxidative stress. The impetus for this review is to highlight neurobiological systems that warrant further evaluation for their contribution to the pathophysiology of depression-cardiovascular disease comorbidity.
压力会引发一系列复杂的神经和外周变化,促进机体对压力的健康适应,但如果压力持续存在,就会导致病理变化。在应对压力源的能力方面,个体之间存在着令人着迷的差异,这使得个体更容易或更不容易患上压力相关的疾病,如抑郁症、焦虑症和心血管疾病。在这篇综述中,我们评估了最近的研究结果,这些结果探讨了在社会挫败压力下采用被动或主动应对策略时的神经基础。因为被动应对与易患与压力相关的疾病有关,而主动应对则赋予了恢复力,因此了解与这些不同应对策略相关的神经生物学适应性可能会揭示出影响压力易感性的生物标志物或靶点。压力引起的抑郁症和心血管疾病的同时发生变得越来越明显。因此,这篇综述的重点是能够导致精神病理学和心血管疾病的中枢机制,如促肾上腺皮质激素释放因子、神经肽 Y、单胺类、细胞因子和氧化应激。撰写这篇综述的动力是强调需要进一步评估神经生物学系统,以了解它们对抑郁症-心血管疾病共病的病理生理学的贡献。