Alvarez Cooper Ignatius, Beecher Kate, Chehrehasa Fatemeh, Belmer Arnauld, Bartlett Selena E
School of Biomedical Sciences, Queensland University of Technology, Brisbane, Australia.
Institute of Health and Biomedical Innovation, Translational Research Institute, Brisbane, Australia.
Brain Plast. 2020 Dec 29;6(1):47-66. doi: 10.3233/BPL-190095.
Alcohol use disorder is a pervasive and detrimental condition that involves changes in neuroplasticity and neurogenesis. Alcohol activates the neuroimmune system and alters the inflammatory status of the brain. Tumour necrosis factor (TNF) is a well characterised neuroimmune signal but its involvement in alcohol use disorder is unknown. In this review, we discuss the variable findings of TNF's effect on neuroplasticity and neurogenesis. Acute ethanol exposure reduces TNF release while chronic alcohol intake generally increases TNF levels. Evidence suggests TNF potentiates excitatory transmission, promotes anxiety during alcohol withdrawal and is involved in drug use in rodents. An association between craving for alcohol and TNF is apparent during withdrawal in humans. While anti-inflammatory therapies show efficacy in reversing neurogenic deficit after alcohol exposure, there is no evidence for TNF's essential involvement in alcohol's effect on neurogenesis. Overall, defining TNF's role in alcohol use disorder is complicated by poor understanding of its variable effects on synaptic transmission and neurogenesis. While TNF may be of relevance during withdrawal, the neuroimmune system likely acts through a larger group of inflammatory cytokines to alter neuroplasticity and neurogenesis. Understanding the individual relevance of TNF in alcohol use disorder awaits a more comprehensive understanding of TNF's effects within the brain.
酒精使用障碍是一种普遍存在且有害的状况，涉及神经可塑性和神经发生的变化。酒精激活神经免疫系统并改变大脑的炎症状态。肿瘤坏死因子（TNF）是一种特征明确的神经免疫信号，但其在酒精使用障碍中的作用尚不清楚。在本综述中，我们讨论了TNF对神经可塑性和神经发生影响的不同研究结果。急性乙醇暴露会减少TNF释放，而长期饮酒通常会增加TNF水平。有证据表明，TNF会增强兴奋性传递，在戒酒期间引发焦虑，并与啮齿动物的药物使用有关。在人类戒酒期间，对酒精的渴望与TNF之间存在明显关联。虽然抗炎疗法在逆转酒精暴露后的神经发生缺陷方面显示出疗效，但没有证据表明TNF在酒精对神经发生的影响中起关键作用。总体而言，由于对TNF对突触传递和神经发生的可变影响了解不足，确定TNF在酒精使用障碍中的作用很复杂。虽然TNF可能在戒酒期间具有相关性，但神经免疫系统可能通过更大一组炎性细胞因子来改变神经可塑性和神经发生。要了解TNF在酒精使用障碍中的个体相关性，还需要更全面地了解TNF在大脑中的作用。
