Department of Psychology, San Diego State University, San Diego, California, USA.
Cognitive and Computational Neuroscience Laboratory, Centre of Biomedical Technology, Madrid, Spain.
Addict Biol. 2021 May;26(3):e12960. doi: 10.1111/adb.12960. Epub 2020 Sep 4.
Animal studies have established that acute alcohol increases neural inhibition and that frequent intoxication episodes elicit neuroadaptive changes in the excitatory/inhibitory neurotransmission balance. To compensate for the depressant effects of alcohol, neural hyperexcitability develops in alcohol use disorder and is manifested through withdrawal symptoms. It is unclear, however, whether neuroadaptive changes can be observed in young, emerging adults at lower levels of consumption in the absence of withdrawal symptoms. Here, we used an anatomically constrained magnetoencephalography method to assess cortical excitability in two independent sets of experiments. We measured early visual activity (1) in social drinkers during alcohol intoxication versus placebo conditions and (2) in parallel cohorts of sober binge drinkers (BDs) and light drinkers (LDs). Acute alcohol intoxication attenuated early sensory activity in the visual cortex in social drinkers, confirming its inhibitory effects on neurotransmission. In contrast, sober BDs showed greater neural responsivity compared with a matched group of LDs. A positive correlation between alcohol consumption and neural activity in BDs is indicative of cortical hyperexcitability associated with hazardous drinking. Furthermore, neural responsivity was positively correlated with alcohol intake in social drinkers whose drinking did not reach binge levels. This study provides novel evidence of compensatory imbalance reflected in the downregulation of inhibitory and upregulation of excitatory signaling associated with binge drinking in young, emerging adults. By contrasting acute effects and a history of BD, these results support the mechanistic model of allostasis. Direct neural measures are sensitive to synaptic currents and could serve as biomarkers of neuroadaptation.
动物研究已经证实，急性酒精会增加神经抑制作用，频繁的醉酒会引起兴奋/抑制性神经递质传递平衡的神经适应性变化。为了补偿酒精的抑制作用，在酒精使用障碍中会出现神经过度兴奋，表现为戒断症状。然而，在没有戒断症状的情况下，在年轻的新兴成年人中，是否可以观察到较低消费水平下的神经适应性变化尚不清楚。在这里，我们使用了一种解剖约束的脑磁图方法在两个独立的实验中评估皮质兴奋性。我们测量了（1）在酒精中毒与安慰剂条件下社交饮酒者的早期视觉活动，以及（2）在清醒 binge 饮酒者（BDs）和轻度饮酒者（LDs）的平行队列中的早期视觉活动。急性酒精中毒会抑制社交饮酒者视觉皮层的早期感觉活动，证实了其对神经传递的抑制作用。相比之下，清醒的 BDs 与匹配的 LDs 相比，表现出更强的神经反应性。BDs 中的酒精消耗与神经活动之间的正相关表明与危险饮酒相关的皮质过度兴奋。此外，在未达到 binge 水平的社交饮酒者中，神经反应性与饮酒量呈正相关。这项研究提供了新的证据，证明了在年轻的新兴成年人中，与 binge 饮酒相关的抑制作用下调和兴奋作用上调所反映的代偿性失衡。通过对比急性效应和 BDs 的历史，这些结果支持了适应的机制模型。直接的神经测量对突触电流敏感，可作为神经适应的生物标志物。
