Indiana University-Purdue University Indianapolis, Department of Psychology, USA.
Indiana University-Purdue University Indianapolis, Department of Psychology, USA.
Neuropharmacology. 2021 Oct 15;198:108780. doi: 10.1016/j.neuropharm.2021.108780. Epub 2021 Sep 1.
Acute ethanol (EtOH) intoxication results in several maladaptive behaviors that may be attributable, in part, to the effects of EtOH on neural activity in medial prefrontal cortex (mPFC). The acute effects of EtOH on mPFC function have been largely described as inhibitory. However, translating these observations on function into a mechanism capable of delineating acute EtOH's effects on behavior has proven difficult. This review highlights the role of acute EtOH on electrophysiological measurements of mPFC function and proposes that interpreting these changes through the lens of dynamical systems theory is critical to understand the mechanisms that mediate the effects of EtOH intoxication on behavior. Specifically, the present review posits that the effects of EtOH on mPFC N-methyl-d-aspartate (NMDA) receptors are critical for the expression of impaired behavior following EtOH consumption. This hypothesis is based on the observation that recurrent activity in cortical networks is supported by NMDA receptors, and, when disrupted, may lead to impairments in cognitive function. To evaluate this hypothesis, we discuss the representation of mPFC neural activity in low-dimensional, dynamic state spaces. This approach has proven useful for identifying the underlying computations necessary for the production of behavior. Ultimately, we hypothesize that EtOH-related alterations to NMDA receptor function produces alterations that can be effectively conceptualized as impairments in attractor dynamics and provides insight into how acute EtOH disrupts forms of cognition that rely on mPFC function. This article is part of the special Issue on 'Neurocircuitry Modulating Drug and Alcohol Abuse'.
急性乙醇（EtOH）中毒会导致多种适应不良行为，部分原因可能是 EtOH 对前额叶皮质（mPFC）的神经活动的影响。EtOH 对 mPFC 功能的急性影响在很大程度上被描述为抑制性的。然而，将这些关于功能的观察结果转化为一种能够阐明急性 EtOH 对行为影响的机制一直很困难。本综述强调了急性 EtOH 对 mPFC 功能的电生理测量的作用，并提出通过动态系统理论的视角来解释这些变化对于理解介导急性 EtOH 中毒对行为影响的机制至关重要。具体来说，本综述假设 EtOH 对 mPFC N-甲基-D-天冬氨酸（NMDA）受体的影响对于解释 EtOH 消耗后行为受损的机制至关重要。这一假设基于以下观察结果：皮质网络中的复发性活动由 NMDA 受体支持，而当 NMDA 受体受到干扰时，可能导致认知功能受损。为了评估这一假设，我们讨论了 mPFC 神经活动在低维动态状态空间中的表示。这种方法已被证明对于识别产生行为所需的基本计算非常有用。最终，我们假设与 EtOH 相关的 NMDA 受体功能改变会产生可以有效概念化为吸引子动力学障碍的改变，并深入了解急性 EtOH 如何破坏依赖 mPFC 功能的认知形式。本文是“神经回路调节药物和酒精滥用”特刊的一部分。
