Article

Why We Like to Drink: A Functional Magnetic Resonance Imaging Study of the Rewarding and Anxiolytic Effects of Alcohol

Laboratory of Clinical and Translational Studies, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland 20892, USA.
The Journal of Neuroscience : The Official Journal of the Society for Neuroscience (Impact Factor: 6.75). 05/2008; 28(18):4583-91. DOI: 10.1523/JNEUROSCI.0086-08.2008
Source: PubMed

ABSTRACT People typically drink alcohol to induce euphoria or reduce anxiety, and they frequently drink in social settings, yet the effect of alcohol on human brain circuits involved in reward and emotion has been explored only sparingly. We administered alcohol intravenously to social drinkers while brain response to visual threatening and nonthreatening facial stimuli was measured using functional magnetic resonance imaging (fMRI). Alcohol robustly activated striatal reward circuits while attenuating response to fearful stimuli in visual and limbic regions. Self-ratings of intoxication correlated with striatal activation, suggesting that activation in this area may contribute to subjective experience of pleasure and reward during intoxication. These results show that the acute pharmacological rewarding and anxiolytic effects of alcohol can be measured with fMRI.

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Available from: Daniel W Hommer, Sep 01, 2015
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    • "Taken together, neuroimaging studies demonstrate the significant influence of alcohol in healthy individuals via alterations in the PSL circuit, including reduced limbic response to negative emotional stimuli (Gilman et al. 2008; Sripada et al. 2011), enhanced striatal response to rewarding stimuli (Filbey et al. 2008; Gilman et al. 2008; Seo et al. 2011) and to risky decisionmaking (Gilman et al. 2012), and impaired episodic memory functioning (Soderlund et al. 2007). These studies clearly point to the PSL circuit as a critical early target of alcohol effects and its potential, deleterious impact on neuroplasticity with chronic alcohol abuse. "
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    ABSTRACT: Chronic alcohol-related neuroadaptations in key neural circuits of emotional and cognitive control play a critical role in the development of, and recovery from, alcoholism. Converging evidence in the neurobiological literature indicates that neuroplastic changes in the prefrontal-striatal-limbic circuit, which governs emotion regulation and decisionmaking and controls physiological responses in the autonomic nervous system and hypothalamic-pituitary-adrenal axis system, contribute to chronic alcoholism and also are significant predictors of relapse and recovery. This paper reviews recent evidence on the neuroplasticity associated with alcoholism in humans, including acute and chronic effects, and how these neurobiological adaptations contribute to alcohol recovery, along with the discussion of relevant clinical implications and future research directions.
    09/2015; 37(1):143-152.
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    • "In an attempt to increase our likelihood of detecting activation differences in smaller brain regions (i.e., amygdala, hippocampus), we set activation thresholds at p = 0.025 with a cluster size threshold of p = 0.10. Therefore, it is possible that our Type I error was inflated, although it is noteworthy that the brain activation pattern differences were consistent with prior studies (Heinz et al., 2007; Li et al., 2005; Salloum et al., 2007) and our resulting volume (1,350 ll) is on par with other imaging studies examining affective processing as well as AD effects (Gilman et al., 2008; Simmons et al., 2008). Second, the current AD sample included individuals x=-7, y=-23, z=-3 t=4.46, p<0.001 "
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    Alcoholism Clinical and Experimental Research 02/2015; 39(2). DOI:10.1111/acer.12626 · 3.31 Impact Factor
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    • "During the alcohol infusion procedure alcohol was infused as a 6% v/v solution in saline to achieve a target breath alcohol concentration (BrAC) of 0.08 g% (AE0.005 g%) in 15 minutes and maintain that concentration for 20 minutes (for further details, see Gilman et al., 2008). Subjective responses to alcohol were measured using the modified Drug Effects Questionnaire (DEQ; de Wit and McCracken , 1990), at baseline (À30 minutes), at the end of the saline phase (À4 minutes), and serially during the infusion at 14, 19, 28, 36, and 50 minutes following the start of the alcohol infusion. "
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    Alcoholism Clinical and Experimental Research 12/2014; 38(12). DOI:10.1111/acer.12581 · 3.31 Impact Factor
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