Understanding ethanol's acute effects on medial prefrontal cortex neural activity using state-space approaches.

Autor: Morningstar MD; Indiana University-Purdue University Indianapolis, Department of Psychology, USA. Electronic address: mdmornin@indiana.edu., Barnett WH; Indiana University-Purdue University Indianapolis, Department of Psychology, USA., Goodlett CR; Indiana University-Purdue University Indianapolis, Department of Psychology, USA; Indiana University School of Medicine, Stark Neurosciences, USA., Kuznetsov A; Indiana University-Purdue University Indianapolis, Department of Mathematics, USA; Indiana University School of Medicine, Stark Neurosciences, USA., Lapish CC; Indiana University-Purdue University Indianapolis, Department of Psychology, USA; Indiana University School of Medicine, Stark Neurosciences, USA.
Jazyk: angličtina
Zdroj: Neuropharmacology [Neuropharmacology] 2021 Oct 15; Vol. 198, pp. 108780. Date of Electronic Publication: 2021 Sep 01.
DOI: 10.1016/j.neuropharm.2021.108780
Abstrakt: 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'.
(Copyright © 2021 Elsevier Ltd. All rights reserved.)
Databáze: MEDLINE
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