Impairment of Neuroplasticity in the Dorsolateral Prefrontal Cortex by Alcohol

Abstract 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 cogn...

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Main Authors: Genane Loheswaran, Mera S. Barr, Reza Zomorrodi, Tarek K. Rajji, Daniel M. Blumberger, Bernard Le Foll, Zafiris J. Daskalakis
Format: Article
Language:English
Published: Nature Portfolio 2017-07-01
Series:Scientific Reports
Online Access:https://doi.org/10.1038/s41598-017-04764-9
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author Genane Loheswaran
Mera S. Barr
Reza Zomorrodi
Tarek K. Rajji
Daniel M. Blumberger
Bernard Le Foll
Zafiris J. Daskalakis
author_facet Genane Loheswaran
Mera S. Barr
Reza Zomorrodi
Tarek K. Rajji
Daniel M. Blumberger
Bernard Le Foll
Zafiris J. Daskalakis
author_sort Genane Loheswaran
collection DOAJ
description Abstract 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.
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spelling doaj-art-233387d4ec6343b58c6c92cbe83294032025-01-26T12:35:24ZengNature PortfolioScientific Reports2045-23222017-07-01711810.1038/s41598-017-04764-9Impairment of Neuroplasticity in the Dorsolateral Prefrontal Cortex by AlcoholGenane Loheswaran0Mera S. Barr1Reza Zomorrodi2Tarek K. Rajji3Daniel M. Blumberger4Bernard Le Foll5Zafiris J. Daskalakis6Translational Addiction Research LaboratoryTemerty Centre for Therapeutic Brain InterventionTemerty Centre for Therapeutic Brain InterventionTemerty Centre for Therapeutic Brain InterventionTemerty Centre for Therapeutic Brain InterventionTranslational Addiction Research LaboratoryTemerty Centre for Therapeutic Brain InterventionAbstract 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.https://doi.org/10.1038/s41598-017-04764-9
spellingShingle Genane Loheswaran
Mera S. Barr
Reza Zomorrodi
Tarek K. Rajji
Daniel M. Blumberger
Bernard Le Foll
Zafiris J. Daskalakis
Impairment of Neuroplasticity in the Dorsolateral Prefrontal Cortex by Alcohol
Scientific Reports
title Impairment of Neuroplasticity in the Dorsolateral Prefrontal Cortex by Alcohol
title_full Impairment of Neuroplasticity in the Dorsolateral Prefrontal Cortex by Alcohol
title_fullStr Impairment of Neuroplasticity in the Dorsolateral Prefrontal Cortex by Alcohol
title_full_unstemmed Impairment of Neuroplasticity in the Dorsolateral Prefrontal Cortex by Alcohol
title_short Impairment of Neuroplasticity in the Dorsolateral Prefrontal Cortex by Alcohol
title_sort impairment of neuroplasticity in the dorsolateral prefrontal cortex by alcohol
url https://doi.org/10.1038/s41598-017-04764-9
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