Citation

Campbell AE, Sumner P, Singh KD, Muthukumaraswamy SD. Neuropsychopharmacology 2014; 39(9): 2104-2113.

Affiliation

CUBRIC, School of Psychology, Cardiff University, Cardiff, UK.

Copyright

(Copyright © 2014, Nature Publishing Group)

DOI

10.1038/npp.2014.58

PMID

24622470

Abstract

Alcohol is a rich drug affecting both the γ-amino butyric acid (GABA) and glutamatergic neurotransmitter systems. Recent findings from both modelling and pharmacological manipulation have indicated a link between GABAergic activity and oscillations measured in the gamma frequency range (30-80 Hz), but there are no previous reports of alcohol's modulation of gamma-band activity measured by magnetoencephalography (MEG) or electroencephalography (EEG). In this single-blind, placebo-controlled crossover study, 16 participants completed two study days, one in which they consumed a dose of 0.8 g/kg alcohol, and the other a placebo. MEG recordings of brain activity were taken before and after beverage consumption, using visual grating and finger abduction paradigms known to induce gamma-band activity in the visual and motor cortices respectively. Time-frequency analyses of beamformer source reconstructions in the visual cortex showed that alcohol increased peak gamma amplitude and decreased peak frequency. For the motor task, alcohol increased gamma amplitude in the motor cortex. These data support the notion that gamma oscillations are dependent, in part, on the balance between excitation and inhibition. Disruption of this balance by alcohol, through increasing GABAergic inhibition at GABAA receptors and decreasing glutamatergic excitation at NMDA receptors, alters both the amplitude and frequency of gamma oscillations. The findings provide further insight into the neuropharmacological action of alcohol.Neuropsychopharmacology accepted article preview online, 13 March 2014; doi:10.1038/npp.2014.58.

Language: en