Translational Addiction Research Laboratory, Toronto Ontario, Canada.
Temerty Centre for Therapeutic Brain Intervention, Toronto Ontario, Canada.
Sci Rep. 2017 Jul 13;7(1):5276. doi: 10.1038/s41598-017-04764-9.
Previous studies have demonstrated that alcohol consumption impairs neuroplasticity in the motor cortex. However, it is unknown whether alcohol produces a similar impairment of neuroplasticity in the dorsolateral prefrontal cortex (DLPFC), a brain region that plays an important role in cognitive functioning. The aim of the current study was to evaluate the effect of alcohol intoxication on neuroplasticity in the DLPFC. Paired associative stimulation (PAS) combined with electroencephalography (EEG) was used for the induction and measurement of associative LTP-like neuroplasticity in the DLPFC. Fifteen healthy subjects were administered PAS to the DLPFC following consumption of an alcohol (1.5 g/l of body water) or placebo beverage in a within-subject cross-over design. PAS induced neuroplasticity was indexed up to 60 minutes following PAS. Additionally, the effect of alcohol on PAS-induced potentiation of theta-gamma coupling (an index associated with learning and memory) was examined prior to and following PAS. Alcohol consumption resulted in a significant impairment of mean (t = 2.456, df = 13, p = 0.029) and maximum potentiation (t = -2.945, df = 13, p = 0.011) compared to the placebo beverage in the DLPFC and globally. Alcohol also suppressed the potentiation of theta-gamma coupling by PAS. Findings from the present study provide a potential neurophysiological mechanism for impairment of cognitive functioning by alcohol.
先前的研究表明，饮酒会损害运动皮层的神经可塑性。然而，目前尚不清楚酒精是否会对背外侧前额叶皮层（DLPFC）产生类似的神经可塑性损伤，而 DLPFC 是大脑中在认知功能中发挥重要作用的区域。本研究的目的是评估酒精中毒对 DLPFC 神经可塑性的影响。采用配对联想刺激（PAS）结合脑电图（EEG），用于诱导和测量 DLPFC 中的联想长时程增强样神经可塑性。15 名健康受试者在摄入含酒精（1.5 g/L 体重水）或安慰剂饮料后，在自身交叉设计中接受 DLPFC 的 PAS。PAS 诱导的神经可塑性在 PAS 后最多 60 分钟进行评估。此外，在 PAS 之前和之后，还检查了酒精对 PAS 诱导的θ-γ耦合增强的影响（与学习和记忆相关的指标）。与安慰剂饮料相比，饮酒导致 DLPFC 和整体的平均（t=2.456，df=13，p=0.029）和最大增强（t=-2.945，df=13，p=0.011）显著受损。酒精还抑制了 PAS 对θ-γ耦合的增强作用。本研究的结果为酒精损害认知功能提供了潜在的神经生理学机制。
