Neurobiological Bases of Alcohol Consumption After Social Stress.
Neurobiological Bases of Alcohol Consumption After Social Stress.
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DOI：
10.1007/7854_2021_273
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发表时间：
2022
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先前的社会压力经历会加剧寻求和过量饮酒的冲动，并且可以在啮齿类动物和非人类灵长类动物的系统控制的实验室条件下对这种级联进行建模。对间歇性社交失败压力的适应性应对通常会转变为对创伤性持续压力的适应不良反应，而饮酒可能成为应对反应的一部分。在回路层面，支持压力应对的神经通路与控制饮酒的神经通路交叉。前额皮质、腹侧和背侧纹状体、丘脑和下丘脑核团、被盖区以及脑干结构内越来越离散的区域和连接开始被认为对于在寻求和饮酒时反应和应对社会压力至关重要。为了减少过度饮酒和复发，已经针对调节这些神经连接内信号的几种候选分子进行了研究。尽管早期的临床试验失败了，但神经肽（如 CRF、阿片类药物或催产素）在减轻压力性饮酒方面的作用仍在继续进行研究。最近的工作重点是肽和类固醇的神经作用位点，最有可能是由于偶发性社会压力和过度饮酒的相互作用而导致的神经炎症过程。
The urge to seek and consume excessive alcohol is intensified by prior experiences with social stress, and this cascade can be modeled under systematically controlled laboratory conditions in rodents and non-human primates. Adaptive coping with intermittent episodes of social defeat stress often transitions to maladaptive responses to traumatic continuous stress, and alcohol consumption may become part of coping responses. At the circuit level, the neural pathways subserving stress coping intersect with those for alcohol consumption. Increasingly discrete regions and connections within the prefrontal cortex, the ventral and dorsal striatum, thalamic and hypothalamic nuclei, tegmental areas as well as brain stem structures begin to be identified as critical for reacting to and coping with social stress while seeking and consuming alcohol. Several candidate molecules that modulate signals within these neural connections have been targeted in order to reduce excessive drinking and relapse. In spite of some early clinical failures, neuropeptides such as CRF, opioids, or oxytocin continue to be examined for their role in attenuating stress-escalated drinking. Recent work has focused on neural sites of action for peptides and steroids, most likely in neuroinflammatory processes as a result of interactive effects of episodic social stress and excessive alcohol seeking and drinking.