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: 6.34). 05/2008; 28(18):4583-91. DOI: 10.1523/JNEUROSCI.0086-08.2008
Source: PubMed


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.

Download full-text


Available from: Daniel W Hommer
  • Source
    • "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. "
    [Show abstract] [Hide abstract]
    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.
    Preview · Article · Sep 2015 · Alcohol research : current reviews
    • "Moreover, alcohol might exert its effects on aggression by increasing dopamine levels in the ventral striatum (Dichiara and Imperato, 1986; Boileau et al, 2003; Heinz et al, 2011), a potential neural mechanism underlying experimentally induced aggression in animals (Miczek et al, 2002; Ferrari et al, 2003; Nelson and Trainor, 2007) and humans (Krämer et al, 2011; Beyer et al, 2014). Using fMRI, alcohol-induced increased dopamine levels might be reflected by increased activation of the ventral striatum in humans (cf, Gilman et al, 2008). However, the interaction between alcohol intoxication and aggression is complex and likely involves other neurotransmitters than dopamine such as serotonin and gamma amino-butyric acid (GABA) (Miczek et al, 2002; Seo et al, 2008; Heinz et al, 2011). "
    [Show abstract] [Hide abstract]
    ABSTRACT: Although alcohol consumption is linked to increased aggression, its neural correlates have not directly been studied in humans so far. Based on a comprehensive neurobiological model of alcohol-induced aggression, we hypothesized that alcohol-induced aggression would go along with increased amygdala and ventral striatum reactivity and impaired functioning of the prefrontal cortex (PFC) under alcohol. We measured neural and behavioral correlates of alcohol-induced aggression in a provoking versus non-provoking condition with a variant of the Taylor aggression paradigm (TAP) allowing to differentiate between reactive (provoked) and proactive (unprovoked) aggression. In a placebo-controlled cross-over design with moderate alcohol intoxication (~0.6 g/kg), thirty-five young healthy adults performed the TAP during functional magnetic resonance imaging (fMRI). Analyses revealed that provoking versus non-provoking conditions and alcohol versus placebo increased aggression, and decreased brain responses in the anterior cingulate cortex/dorso-medial PFC (provoking<non-provoking), and the ventral striatum (alcohol<placebo) across our healthy sample. Interestingly, alcohol specifically increased pro-active (unprovoked) but not reactive (provoked) aggression (alcohol x provocation interaction). However, investigation of inter-individual differences revealed (1) that pronounced alcohol-induced pro-active aggression was linked to higher levels of aggression under placebo, and (2) that pronounced alcohol-induced reactive aggression was related to increased amygdala and ventral striatum reactivity under alcohol, providing evidence for their role in human alcohol-induced reactive aggression. Our findings suggest that in healthy young adults a liability for alcohol-induced aggression in a non-provoking context might depend on overall high levels of aggression, but on alcohol-induced increased striatal and amygdala reactivity when triggered by provocation.
    No preview · Article · May 2015 · Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology
  • Source
    • "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 "
    [Show abstract] [Hide abstract]
    ABSTRACT: Background Alcohol dependence (AD) has global effects on brain structure and function, including frontolimbic regions regulating affective processing. Preliminary evidence suggests alcohol blunts limbic response to negative affective stimuli and increases activation to positive affective stimuli. Subtle gender differences are also evident during affective processing.Methods Fourteen abstinent AD individuals (8 F, 6 M) and 14 healthy controls (9 F, 5 M), ages 23 to 60, were included in this facial affective processing functional magnetic resonance imaging pilot study. Whole-brain linear regression analyses were performed, and follow-up analyses examined whether AD status significantly predicted depressive symptoms and/or coping.ResultsFearful Condition—The AD group demonstrated reduced activation in the right medial frontal gyrus, compared with controls. Gender moderated the effects of AD in bilateral inferior frontal gyri. Happy Condition—AD individuals had increased activation in the right thalamus. Gender moderated the effects of AD in the left caudate, right middle frontal gyrus, left paracentral lobule, and right lingual gyrus. Interactive AD and gender effects for fearful and happy faces were such that AD men activated more than control men, but AD women activated less than control women. Enhanced coping was associated with greater activation in right medial frontal gyrus during fearful condition in AD individuals.Conclusions Abnormal affective processing in AD may be a marker of alcoholism risk or a consequence of chronic alcoholism. Subtle gender differences were observed, and gender moderated the effects of AD on neural substrates of affective processing. AD individuals with enhanced coping had brain activation patterns more similar to controls. Results help elucidate the effects of alcohol, gender, and their interaction on affective processing.
    Full-text · Article · Feb 2015 · Alcoholism Clinical and Experimental Research
Show more