The role of the gut-brain axis in alcohol use disorders.
The role of the gut-brain axis in alcohol use disorders.
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DOI：
10.1016/j.pnpbp.2015.06.013
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发表时间：
2016-02-04
影响因子：
5.6
通讯作者：
Schwaber J
中科院分区：
文献类型：
--
作者：
Gorky J;Schwaber J
在酒精暴露和戒断过程中，神经免疫和炎症过程与杏仁核局部相关。我们和其他人已经提出，杏仁核中的这种炎症可能会导致神经功能紊乱，在戒断过程中表现为焦虑和自主神经痛苦。尽管强大的神经炎性反应具有潜在的重要性，但对这种反应的机制还不是很清楚。我们回顾了一些文献，这些文献表明酒精和其他滥用物质的影响会导致肠道微生物群的失调。这种外周反应可能调节神经保护性迷走神经传入信号，从而允许并加剧杏仁核的神经炎性反应。我们将研究越来越多的证据表明：(1)肠道生物失调导致神经炎症，特别是在酒精暴露和戒断的背景下；(2)杏仁核的神经炎症涉及小胶质细胞和星形胶质细胞及其对神经细胞的影响；(3)杏仁核神经炎症本身直接导致戒断行为和症状。肠道对焦虑性反应的贡献对于患有戒断症状的患者来说是一个有希望的治疗目标，因为有安全和成熟的肠道微生物群调节方法。
Neuroimmune and inflammatory processes have been locally associated with the amygdala in alcohol exposure and withdrawal. We and others have suggested that this inflammation in the amygdala may cause disturbance of neural function observed as anxiety and autonomic distress in withdrawal. Despite the potential importance of the robust neuroinflammatory response, the mechanisms contributing to this response are not well understood. We review literature that suggests the effects of alcohol, and other substances of abuse, cause dysbiosis of the gut microbiome. This peripheral response may modulate neuroprotective vagal afferent signaling that permits and exacerbates a neuroinflammatory response in the amygdala. We will examine the mounting evidence that suggests that (1) gut dysbiosis contributes to neuroinflammation, especially in the context of alcohol exposure and withdrawal, (2) the neuroinflammation in the amygdala involves the microglia and astrocytes and their effect on neural cells, and (3) amygdala neuroinflammation itself contributes directly to withdrawal behavior and symptoms. The contribution of the gut to an anxiogenic response is a promising therapeutic target for patients suffering with withdrawal symptoms given the safe and well-established methods of modulating the gut microbiome.