Preprint Article Version 1 Preserved in Portico This version is not peer-reviewed

Disinhibited-Like Behavior Correlates With Frontal Cortex Damage in Alcohol-Induced Wernicke-Korsakoff Syndrome

Version 1 : Received: 24 November 2021 / Approved: 25 November 2021 / Online: 25 November 2021 (16:03:13 CET)

How to cite: Moya, M.; López-Valencia, L.; García-Bueno, B.; Orio, L. Disinhibited-Like Behavior Correlates With Frontal Cortex Damage in Alcohol-Induced Wernicke-Korsakoff Syndrome. Preprints 2021, 2021110484 (doi: 10.20944/preprints202111.0484.v1). Moya, M.; López-Valencia, L.; García-Bueno, B.; Orio, L. Disinhibited-Like Behavior Correlates With Frontal Cortex Damage in Alcohol-Induced Wernicke-Korsakoff Syndrome. Preprints 2021, 2021110484 (doi: 10.20944/preprints202111.0484.v1).

Abstract

Wernicke-Korsakoff syndrome (WKS) is induced by thiamine deficiency (TD) and mainly related to alcohol consumption. Frontal cortex dysfunction has been associated to impulsivity and disinhibition in WKS patients. The pathophysiology involves oxidative stress, excitotoxicity and inflammatory responses leading to neuronal death, but the relative contributions of each factor (alcohol and TD, isolate or in interaction) to these phenomena are still poorly understood. A rat model was used by forced consumption of 20% (w/v) alcohol for 9 months (CA), TD hit (TD diet + pyrithiamine 0.25 mg/kg, i.p. daily injections the last 12 days of experimentation; TDD), and both combined treatments (CA+TDD). Motor and cognitive performance and cortical damage were examined. CA caused hyperlocomotion as a possible sensitization of ethanol-induced excitatory effects and recognition memory deficits. In addition, CA+TDD animals showed a disinhibited-like behavior, which appears to be dependent on TDD. Also, combined treatment led to more pronounced alterations in nitrosative stress, lipid peroxidation, apoptosis and cell damage markers. Correlations between injury signals and disinhibition suggest that CA+TDD disrupts behaviors dependent on the frontal cortex. Our study sheds light on the potential disease-specific mechanisms, reinforcing the need for neuroprotective therapeutic approaches along with preventive treatments for the nutritional deficiency in WKS.

Keywords

Chronic alcohol; Thiamine Deficiency; Disinhibition; Wernicke´s Encephalopathy; Recognition memory; Nitrosative stress; Lipid peroxidation; Apoptosis; Cell damage; Nutritional deficit

Subject

BEHAVIORAL SCIENCES, Behavioral Neuroscience

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