Alcohol impacts an fMRI marker of neural inhibition in humans and rodents.

Abstract

Acute alcohol consumption leads to cognitive and behavioral disinhibition that increase health and social risks, such as traffic fatalities and violence. Although rodent studies have shown that alcohol affects inhibitory neuronal activity, its relevance to humans remains largely unexplored. Here, we used the Hurst exponent--an fMRI-based marker of neural inhibition--to examine alcohols effects in both rats and humans. In rats, acute alcohol administration significantly reduced the cortical Hurst exponent, suggesting a decrease in inhibitory neuronal activity. This reduction was strongly correlated with the spatial distribution of GABAA receptor expression, highlighting the key role of these receptors in mediating alcohols effects. Similarly, in humans, acute alcohol consumption reduced the cortical Hurst exponent, especially in brain regions with high GABAA receptor expression. Our findings provide cross-species in vivo evidence that acute alcohol consumption modulates neural inhibition, offering new insights into the neural mechanisms underlying alcohol-induced behavioral modulation.