The role of neuroimmune signaling in alcoholism

被引:223
作者
Crews, Fulton T. [1 ]
Lawrimore, Colleen J. [1 ]
Walter, T. Jordan [1 ]
Coleman, Leon G., Jr. [1 ]
机构
[1] Univ N Carolina, Chapel Hill Sch Med, Bowles Ctr Alcohol Studies, CB 7178 UNC CH, Chapel Hill, NC 27599 USA
关键词
HMGB1; TLR; Cytokines; miRNA-let-7; Alcohol; Addiction; NF-KAPPA-B; INTERMITTENT ETHANOL EXPOSURE; ADULT HIPPOCAMPAL NEUROGENESIS; NEURO-IMMUNOLOGICAL FACTORS; PRO-INFLAMMATORY CYTOKINES; ACUTE PSYCHOLOGICAL STRESS; DEPRESSION-LIKE BEHAVIOR; TRAUMATIC BRAIN-INJURY; TOLL-LIKE RECEPTORS; NUCLEAR-FACTOR;
D O I
10.1016/j.neuropharm.2017.01.031
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Alcohol consumption and stress increase brain levels of known innate immune signaling molecules. Microglia, the innate immune cells of the brain, and neurons respond to alcohol, signaling through Toll like receptors (TLRs), high-mobility group box 1 (HMGB1), miRNAs, pro-inflammatory cytokines and their associated receptors involved in signaling between microglia, other glia and neurons. Repeated cycles of alcohol and stress cause a progressive, persistent induction of HMGB1, miRNA and TLR receptors in brain that appear to underlie the progressive and persistent loss of behavioral control, increased impulsivity and anxiety, as well as craving, coupled with increasing ventral striatal responses that promote reward seeking behavior and increase risk of developing alcohol use disorders. Studies employing anti-oxidant, anti-inflammatory, anti-depressant, and innate immune antagonists further link innate immune gene expression to addiction-like behaviors. Innate immune molecules are novel targets for addiction and affective disorders therapies. This article is part of the Special Issue entitled "Alcoholism". (C) 2017 Elsevier Ltd. All rights reserved.
引用
收藏
页码:56 / 73
页数:18
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