Shokri-Kojori E, Tomasi D, Wiers C E, Wang G-J, Volkow N D
Laboratory of Neuroimaging, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA.
National Institute on Drug Abuse, National Institutes of Health, Bethesda, MD, USA.
Mol Psychiatry. 2017 Aug;22(8):1185-1195. doi: 10.1038/mp.2016.25. Epub 2016 Mar 29.
Acute and chronic alcohol exposure significantly affect behavior but the underlying neurobiological mechanisms are still poorly understood. Here, we used functional connectivity density (FCD) mapping to study alcohol-related changes in resting brain activity and their association with behavior. Heavy drinkers (HD, N=16, 16 males) and normal controls (NM, N=24, 14 males) were tested after placebo and after acute alcohol administration. Group comparisons showed that NM had higher FCD in visual and prefrontal cortices, default mode network regions and thalamus, while HD had higher FCD in cerebellum. Acute alcohol significantly increased FCD within the thalamus, impaired cognitive and motor functions, and affected self-reports of mood/drug effects in both groups. Partial least squares regression showed that alcohol-induced changes in mood/drug effects were associated with changes in thalamic FCD in both groups. Disruptions in motor function were associated with increases in cerebellar FCD in NM and thalamus FCD in HD. Alcohol-induced declines in cognitive performance were associated with connectivity increases in visual cortex and thalamus in NM, but in HD, increases in precuneus FCD were associated with improved cognitive performance. Acute alcohol reduced 'neurocognitive coupling', the association between behavioral performance and FCD (indexing brain activity), an effect that was accentuated in HD compared with NM. Findings suggest that reduced cortical connectivity in HD contribute to decline in cognitive abilities associated with heavy alcohol consumption, whereas increased cerebellar connectivity in HD may have compensatory effects on behavioral performance. The results reveal how drinking history alters the association between brain FCD and individual differences in behavioral performance.
急性和慢性酒精暴露会显著影响行为,但其潜在的神经生物学机制仍知之甚少。在此,我们使用功能连接密度(FCD)映射来研究静息脑活动中与酒精相关的变化及其与行为的关联。对重度饮酒者(HD,N = 16,16名男性)和正常对照组(NM,N = 24,14名男性)在服用安慰剂后和急性酒精给药后进行了测试。组间比较显示,NM在视觉和前额叶皮层、默认模式网络区域及丘脑中具有较高的FCD,而HD在小脑中具有较高的FCD。急性酒精显著增加了丘脑中的FCD,损害了认知和运动功能,并影响了两组的情绪/药物效应自我报告。偏最小二乘回归显示,两组中酒精诱导的情绪/药物效应变化与丘脑FCD的变化相关。运动功能障碍与NM组小脑中FCD的增加以及HD组丘脑中FCD的增加相关。酒精诱导的认知表现下降与NM组视觉皮层和丘脑中连接性的增加相关,但在HD组中,楔前叶FCD的增加与认知表现的改善相关。急性酒精降低了“神经认知耦合”,即行为表现与FCD(指示脑活动)之间的关联,与NM组相比,HD组的这种效应更为明显。研究结果表明,HD组皮层连接性降低导致与大量饮酒相关的认知能力下降,而HD组小脑中连接性增加可能对行为表现具有补偿作用。结果揭示了饮酒史如何改变脑FCD与行为表现个体差异之间的关联。