Article

Dysfunction of reward processing correlates with alcohol craving in detoxified alcoholics

Ruhr-Universität Bochum, Bochum, North Rhine-Westphalia, Germany
NeuroImage (Impact Factor: 6.13). 05/2007; 35(2):787-94. DOI: 10.1016/j.neuroimage.2006.11.043
Source: PubMed

ABSTRACT Alcohol dependence may be associated with dysfunction of mesolimbic circuitry, such that anticipation of nonalcoholic reward fails to activate the ventral striatum, while alcohol-associated cues continue to activate this region. This may lead alcoholics to crave the pharmacological effects of alcohol to a greater extent than other conventional rewards. The present study investigated neural mechanisms underlying these phenomena.
16 detoxified male alcoholics and 16 age-matched healthy volunteers participated in two fMRI paradigms. In the first paradigm, alcohol-associated and affectively neutral pictures were presented, whereas in the second paradigm, a monetary incentive delay task (MID) was performed, in which brain activation during anticipation of monetary gain and loss was examined. For both paradigms, we assessed the association of alcohol craving with neural activation to incentive cues.
Detoxified alcoholics showed reduced activation of the ventral striatum during anticipation of monetary gain relative to healthy controls, despite similar performance. However, alcoholics showed increased ventral striatal activation in response to alcohol-associated cues. Reduced activation in the ventral striatum during expectation of monetary reward, and increased activation during presentation of alcohol cues were correlated with alcohol craving in alcoholics, but not healthy controls.
These results suggest that mesolimbic activation in alcoholics is biased towards processing of alcohol cues. This might explain why alcoholics find it particularly difficult to focus on conventional reward cues and engage in alternative rewarding activities.

2 Followers
 · 
281 Views
  • [Show abstract] [Hide abstract]
    ABSTRACT: The default mode network is associated with senior cognitive functions in humans. In this study, we performed independent component analysis of blood oxygenation signals from 14 heroin users and 13 matched normal controls in the resting state through functional MRI scans. Results showed that the default mode network was significantly activated in the prefrontal lobe, posterior cingulated cortex and hippocampus of heroin users, and an enhanced activation signal was observed in the right inferior parietal lobule (P < 0.05, corrected for false discovery rate). Experimental findings indicate that the default mode network is altered in heroin users.
    Neural Regeneration Research 06/2012; 7(18):1386-91. DOI:10.3969/j.issn.1673-5374.2012.18.004 · 0.23 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Drugs of abuse elicit dopamine release in the ventral striatum, possibly biasing dopamine-driven reinforcement learning towards drug-related reward at the expense of non-drug-related reward. Indeed, in alcohol-dependent patients, reactivity in dopaminergic target areas is shifted from non-drug-related stimuli towards drug-related stimuli. Such ‘hijacked’ dopamine signals may impair flexible learning from non-drug-related rewards, and thus promote craving for the drug of abuse. Here, we used functional magnetic resonance imaging to measure ventral striatal activation by reward prediction errors (RPEs) during a probabilistic reversal learning task in recently detoxified alcohol-dependent patients and healthy controls (N = 27). All participants also underwent 6-[18F]fluoro-DOPA positron emission tomography to assess ventral striatal dopamine synthesis capacity. Neither ventral striatal activation by RPEs nor striatal dopamine synthesis capacity differed between groups. However, ventral striatal coding of RPEs correlated inversely with craving in patients. Furthermore, we found a negative correlation between ventral striatal coding of RPEs and dopamine synthesis capacity in healthy controls, but not in alcohol-dependent patients. Moderator analyses showed that the magnitude of the association between dopamine synthesis capacity and RPE coding depended on the amount of chronic, habitual alcohol intake. Despite the relatively small sample size, a power analysis supports the reported results. Using a multimodal imaging approach, this study suggests that dopaminergic modulation of neural learning signals is disrupted in alcohol dependence in proportion to long-term alcohol intake of patients. Alcohol intake may perpetuate itself by interfering with dopaminergic modulation of neural learning signals in the ventral striatum, thus increasing craving for habitual drug intake.
    European Journal of Neuroscience 12/2014; 41(4). DOI:10.1111/ejn.12802 · 3.67 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: El cannabis es una de las drogas de abuso más frecuentes. Afecta al sistema de recompensa cerebral en los animales, y tiene un potencial de recompensa y adicción demostrado en el ser humano. Hemos utilizado la RM funcional para medir la actividad cerebral durante la anticipación de la recompensa en una tarea de recompensa monetaria. Se comparó a consumidores crónicos de cannabis con individuos de control sanos. Se utilizó otro grupo control adicional formado por consumidores de nicotina. Los consumidores de cannabis mostraron una actividad cerebral atenuada durante la anticipación de la recompensa en el núcleo accumbens, en comparación con los controles no fumadores, pero no en comparación con los controles fumadores. Los consumidores de cannabis mostraron una reducción de la actividad de anticipación de recompensa en el núcleo caudado, en comparación con los controles tanto fumadores como no fumadores. Estos datos sugieren que la nicotina puede ser responsable de una atenuación de la actividad de anticipación de recompensa en el núcleo accumbens, pero que las diferencias que se producen en el caudado se asocian al consumo de cannabis. Nuestros resultados implican que el consumo crónico de cannabis, así como el de nicotina, puede causar una alteración de la respuesta cerebral a los estímulos de recompensa.
    04/2011; 18(2):45-54. DOI:10.1016/j.psiq.2011.08.003