Alcohol Intoxication by Binge Drinking Impairs Neuroplasticity.

Abstract

Binge drinking, resulting in acute alcohol intoxication, is considered an initial step in developing alcohol use disorders (AUDs). It has been suggested that alcohol intoxication may act on mechanisms of neuroplasticity to produce brain changes that contribute to the pathophysiology of AUDs. However, the effect of binge drinking on neuroplasticity has not been evaluated in humans. The current study was aimed at evaluating the effect of a binge drinking episode on LTP-like neuroplasticity. In a within-subject randomized, cross-over design, fifteen otherwise healthy binge drinkers were administered paired associative stimulation (PAS) following consumption of alcohol or a placebo beverage. PAS is an experimental paradigm that allows for the induction of associative long-term potentiation (LTP)-like neuroplasticity. Subjects were administered alcohol at a dose of 1.5 g/l of body water, producing a peak blood alcohol concentration (BAC) of 26.1 mM (0.120% BAC). PAS induced neuroplasticity was measured at Post 0 (immediately following PAS), Post 15 (15 minutes following PAS), Post 30 (30 minutes following PAS), Post 60 (60 minutes following PAS) and Post Day 1 (the next day following PAS). The binge drinking episode inhibited LTP-like neuroplasticity, which was significantly different from placebo at 30 and 60 min following the PAS administration. Examination of longitudinal effects revealed no differences between beverages on LTP-like neuroplasticity the following day. Findings suggest that binge drinking impairs neuroplasticity and while these effects are no longer evident the day after a single binge session, repetitive binging may produce long lasting changes in neuroplasticity that contribute to the development of AUDs.