Impairment of Neuroplasticity in the Dorsolateral Prefrontal Cortex by Alcohol

• Published in: Scientific reports Vol. 7; no. 1; pp. 5276 - 8
• Main Authors: Loheswaran, Genane, Barr, Mera S., Zomorrodi, Reza, Rajji, Tarek K., Blumberger, Daniel M., Le Foll, Bernard, Daskalakis, Zafiris J.
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 13.07.2017; Nature Publishing Group; Nature Portfolio
• Subjects: 631/378/2591/2592; 631/443/376; Adult; Alcohol; Alcohol use; Alcoholic beverages; Alcoholic Intoxication - etiology; Alcoholic Intoxication - pathology; Alcohols; Body water; Central Nervous System Depressants - adverse effects; Cognitive ability; Cortex (motor); Cross-Over Studies; EEG; Ethanol - adverse effects; Evoked Potentials, Motor - drug effects; Female; Humanities and Social Sciences; Humans; Intoxication; Learning; Long-term potentiation; Male; Memory; Middle Aged; multidisciplinary; Neuronal Plasticity; Neuroplasticity; Placebos; Prefrontal cortex; Prefrontal Cortex - drug effects; Prefrontal Cortex - pathology; Science; Science (multidisciplinary); Transcranial Magnetic Stimulation; Young Adult
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/s41598-017-04764-9

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.