Chronic Alcohol Intake During Adolescence, but not Adulthood, Promotes Persistent Deficits in Risk-Based Decision Making

Schindler, Abigail G.; Tsutsui, Kimberly T.; Clark, Jeremy J.

doi:10.1111/acer.12404

Cited by 64 publications

(75 citation statements)

References 53 publications

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“…Importantly, a previous study in which rats were pair-housed and exposed to intragastric alcohol or control administration during adolescence observed that alcohol-treated animals showed increased lever-pressing behavior during Pavlovian conditioning consistent with the results outlined here (McClory and Spear, 2014), indicating that the effects of alcohol on learning are consistent across housing conditions. Finally, our work demonstrating that adolescent alcohol promotes maladaptive decision making (Nasrallah et al, 2011;Schindler et al, 2014), findings that we have previously linked to learning effects similar to the ones found here (Clark et al, 2012), have been replicated in animals that were group housed during intragastric alcohol administration in adolescence (Boutros et al, 2014). Thus the observed increase in sign-tracking behavior reported here is most likely the result of alcohol exposure rather than housing conditions.…”

Section: Discussionsupporting

confidence: 82%

“…Daily adolescent alcohol intake was stable across the 20-day exposure period (F (19,266) day = 1.62, NS) and averaged 11.5 ± 0.98 g/kg, comparable to our previous studies ( Figure 1b; Nasrallah et al, 2011;Schindler et al, 2014). The caloric intake was comparable for alcohol-and controlexposed animals (F (6,172) day × group = 1.69, NS; F (1,29) group = 0.184, NS) and both groups increased in body weight to the same extent over the course of the 20-day exposure period (Figure 1c; F (1,35) day × group = 1.57, NS; F (1,29) group = 1.48, NS).…”

Section: Alcohol Intakesupporting

confidence: 90%

“…We have further demonstrated that increased risk preference may result from a selective defect in reinforcement learning (Clark et al, 2012) and that this is a specific consequence of alcohol exposure during adolescence, as identical exposure in adults does not produce this effect (Schindler et al, 2014). The mesolimbic dopamine system is implicated in reinforcement learning, goal-directed behavior, and motivational processes, including those for abused substances (Everitt and Robbins, 2005;Kelley, 2004;Robinson and Berridge, 1993;Salmone and Correa, 2012;Schultz, 2007).…”

Section: Introductionmentioning

confidence: 79%

“…Therefore, any measure of BEC is likely to be a systematic underestimate because the average BEC will include animals that do not consume alcohol during the sampling period chosen. However, we have previously examined BEC after alcohol gelatin exposure during adolescence (Schindler et al, 2014) as have others (Rowland et al, 2005;McMurray et al, 2014). To assess BEC, we isolated peak intake periods to get an accurate estimate given a specific amount of intake.…”

Section: Alcohol Administrationmentioning

confidence: 99%

“…Alcohol is the most commonly used substance by adolescents and a high percentage of consumption during this period occurs in bingeing or uncontrolled use (Witt, 2010). Importantly, an increasing number of studies have revealed that the adolescent brain is particularly vulnerable to alcohol-induced functional changes (Crews et al, 2007;Guerri and Pascual 2010;Monti et al, 2005;Philpot et al, 2009;Schindler et al, 2014;Squeglia et al, 2012;Zeigler et al, 2005). Moreover, adolescent alcohol use increases the likelihood of developing an alcohol use disorder (AUD) in adulthood (Blomeyer et al, 2013;Dawson et al, 2008;Hingson et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

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Adolescent Alcohol Exposure Amplifies the Incentive Value of Reward-Predictive Cues Through Potentiation of Phasic Dopamine Signaling

Spoelder

Tsutsui

Lesscher

et al. 2015

Neuropsychopharmacol

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Adolescent alcohol use remains a major public health concern due in part to well-established findings implicating the age of onset in alcohol use in the development of alcohol use disorders and persistent decision-making deficits in adults. We have previously demonstrated that moderate adolescent alcohol consumption in rats promotes suboptimal decision making and an associated perturbation in mesolimbic dopamine transmission in adulthood. Dopamine-dependent incentive learning processes are an integral component of value-based decision making and a fundamental element to many theoretical accounts of addiction. Thus we tested the hypothesis that adolescent alcohol use selectively alters incentive learning processes through perturbation of mesolimbic dopamine systems. To assess incentive learning, behavioral and neurochemical measurements were made during the acquisition, maintenance, extinction, and reacquisition of a Pavlovian conditioned approach procedure in adult rats with a history of adolescent alcohol consumption. We show that moderate adolescent alcohol consumption potentiates stimulus-evoked phasic dopamine transmission, measured in vivo by fast-scan cyclic voltammetry, in adulthood and biases individuals toward a dopamine-dependent incentive learning strategy. Moreover, we demonstrate that animals exposed to alcohol in adolescence are more sensitive to an unexpected variation in reward outcomes. This pattern of phasic dopamine signaling and the associated bias in learning may provide a mechanism for the well-documented vulnerability of individuals with early-life alcohol use for alcohol use disorders in adulthood.

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Section: Discussionsupporting

confidence: 82%

Section: Alcohol Intakesupporting

confidence: 90%

Section: Introductionmentioning

confidence: 79%

Section: Alcohol Administrationmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Adolescent Alcohol Exposure Amplifies the Incentive Value of Reward-Predictive Cues Through Potentiation of Phasic Dopamine Signaling

Spoelder

Tsutsui

Lesscher

et al. 2015

Neuropsychopharmacol

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The impact of junk foods on the adolescent brain

Reichelt

Rank

2017

Birth Defects Research

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Adolescence is a significant period of physical, social, and emotional development, and is characterized by prominent neurobiological changes in the brain. The maturational processes that occur in brain regions responsible for cognitive control and reward seeking may underpin excessive consumption of palatable high fat and high sugar "junk" foods during adolescence. Recent studies have highlighted the negative impact of these foods on brain function, resulting in cognitive impairments and altered reward processing. The increased neuroplasticity during adolescence may render the brain vulnerable to the negative effects of these foods on cognition and behavior. In this review, we describe the mechanisms by which junk food diets influence neurodevelopment during adolescence. Diet can lead to alterations in dopamine-mediated reward signaling, and inhibitory neurotransmission controlled by γ-aminobutyric acid (GABA), two major neurotransmitter systems that are under construction across adolescence. We propose that poor dietary choices may derail the normal adolescent maturation process and influence neurodevelopmental trajectories, which can predispose individuals to dysregulated eating and impulsive behaviors.

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