Abstract
main mechanisms via which alcohol intoxication can alter behavior and cognition: Globally speaking, one would expect an unspecific dysfunction of higher-order cogni-tion due to the reduction in a mainly excitatory transmit-ter (glutamate) and the boosting of a mainly inhibitory transmitter (GABA). More specifically, one would expect changes in executive functions. Executive functions that can be altered by alcohol comprise response inhibition, task selection, task switching, and response monitoring (Goldstein and Volkow 2011). There are many studies and reviews substantiating a decline of executive functioning in long-term alcohol abuse (e.g., Oscar-Berman 2012), and more recent studies have started to demonstrate simi-lar effects in frequent binge drinkers, although to a lesser extent and with more mixed results (see Montgomery et al. 2012). Yet, there is a marked scarcity of studies investi-gating the acute effects of a heavy (binge-like) intoxica-tion. The shortage of such studies poses a problem when it comes to logically linking acute to long-term conse-quences of increased alcohol consumption in the form of binge drinking.Hence, very little is known about whether behavioral (executive) deficits observed during a pronounced intoxica-tion are the result of a global and unspecific “dampening” of cognitive functions or rather the consequence of deficits in a distinct subset of cognitive subprocesses contributing to behavior. Executive functions are mediated via loops interconnecting the PFC and the basal ganglia (which have been shown to heavily depend the proper functioning of GABAergic and dopaminergic signaling; see Plenz 2003; Beste etal. 2009). The high complexity of these fronto-striatal loops, the fact that different cognitive functions rely on the integrity of different transmitter systems, and the finding that cognitive subprocesses can be differentiated using experimental psychological and neurophysiological Alcohol is a common drug of abuse and the adverse effects of chronic overconsumption are well known (e.g., Fadda and Rossetti 1998). However, drinking patterns and hab-its have started to change drastically, especially among younger people in Western cultures (Jernigan 2001; Mont-gomery et al. 2012). In this context, the term “binge drink-ing” describes a drinking pattern that is characterized by the consumption of alcoholic beverages with the primary intention of reaching a marked intoxication (as character-ized by a blood alcohol concentration of at least 0.8‰). For adult males, it takes at least five standard drinks, and for adult females, it takes at least four drinks to achieve this level of intoxication (Crabbe et al. 2011). The most striking differences between binge drinking and “traditional” alco-holism are the irregularity of alcohol intake and the young age of consumers (Hermens et al. 2013). Since the prefron-tal cortex (PFC) is subject to development and maturation during adolescence and emerging adulthood, binge drink-ing until the age of 24 probably poses a bigger harm to proper executive functioning than it does in later stages of life (Hermens et al. 2013).To better understand the effects of binge drinking, one must take a closer look at the acute neurobiological changes it induces. During acute alcohol intoxication, several neurotransmitter systems are subject to changes. While glutamatergic neurotransmission is downregulated, signaling via GABA, dopamine, serotonin, and opioid pep -tides becomes enhanced (Clapp et2008 al. ). Even though this list of changes is not comprehensive, it suggests two
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