Dataset Information

Cognitive control links alcohol use, trait disinhibition, and reduced cognitive capacity: Evidence for medial prefrontal cortex dysregulation during reward-seeking behavior.

ABSTRACT:

Background

Guided by the prediction of response-outcome theory of cognitive control (Alexander and Brown, 2010a), the present study examined reward-seeking medial prefrontal cortex (mPFC) activity as a common neuro-functional marker of excessive alcohol consumption, trait disinhibition, and reduced cognitive capacity; all of which have shown consistent patterns of covariation in previous psychometric research (e.g., Bogg and Finn, 2010).

Methods

A sample of 18-23-year-old university students with a heterogeneous prevalence of alcohol dependence was assessed with functional magnetic resonance imaging (fMRI) while completing a version of the Balloon Analogue Risk Task (Lejuez et al., 2002). A follow-back typical weekly alcohol consumption interview, self-report measures of trait disinhibition and IQ, and a complex span working memory task also were administered.

Results

Correlational region-of-interest analyses showed greater typical weekly alcohol consumption, greater trait disinhibition, and lower IQ were associated with greater reductions in mPFC activity during reward-seeking behaviors (successive inflation choices). The results also showed greater typical weekly alcohol consumption, greater trait disinhibition, and lower IQ were associated with greater increases in mPFC activity during reward-seeking outcomes (successive successful inflation outcomes). No significant relations with the measure of working memory were found.

Conclusions

The findings suggest mPFC activity during risk/reward appraisal and performance monitoring is a common neuro-functional feature of co-varying expressions of excessive alcohol consumption, trait disinhibition, and lower IQ.

SUBMITTER: Bogg T

PROVIDER: S-EPMC3258478 | biostudies-literature | 2012 Apr

REPOSITORIES: biostudies-literature

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Publications

Cognitive control links alcohol use, trait disinhibition, and reduced cognitive capacity: Evidence for medial prefrontal cortex dysregulation during reward-seeking behavior.

Bogg Tim T Fukunaga Rena R Finn Peter R PR Brown Joshua W JW

Drug and alcohol dependence 20111010 1-2

<h4>Background</h4>Guided by the prediction of response-outcome theory of cognitive control (Alexander and Brown, 2010a), the present study examined reward-seeking medial prefrontal cortex (mPFC) activity as a common neuro-functional marker of excessive alcohol consumption, trait disinhibition, and reduced cognitive capacity; all of which have shown consistent patterns of covariation in previous psychometric research (e.g., Bogg and Finn, 2010).<h4>Methods</h4>A sample of 18-23-year-old universi ...[more]

PMID: 21992873

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Project description:Major depressive disorder is a leading cause of disability and significant mortality, yet mechanistic understanding remains limited. Over the past decade evidence has accumulated from case-control studies that depressive illness is associated with blunted reward activation in the basal ganglia and other regions such as the medial prefrontal cortex. However it is unclear whether this finding can be replicated in a large number of subjects. The functional anatomy of the medial prefrontal cortex and basal ganglia has been extensively studied and the former has excitatory glutamatergic projections to the latter. Reduced effect of glutamatergic projections from the prefrontal cortex to the nucleus accumbens has been argued to underlie motivational disorders such as depression, and many prominent theories of major depressive disorder propose a role for abnormal cortico-limbic connectivity. However, it is unclear whether there is abnormal reward-linked effective connectivity between the medial prefrontal cortex and basal ganglia related to depression. While resting state connectivity abnormalities have been frequently reported in depression, it has not been possible to directly link these findings to reward-learning studies. Here, we tested two main hypotheses. First, mood symptoms are associated with blunted striatal reward prediction error signals in a large community-based sample of recovered and currently ill patients, similar to reports from a number of studies. Second, event-related directed medial prefrontal cortex to basal ganglia effective connectivity is abnormally increased or decreased related to the severity of mood symptoms. Using a Research Domain Criteria approach, data were acquired from a large community-based sample of subjects who participated in a probabilistic reward learning task during event-related functional MRI. Computational modelling of behaviour, model-free and model-based functional MRI, and effective connectivity dynamic causal modelling analyses were used to test hypotheses. Increased depressive symptom severity was related to decreased reward signals in areas which included the nucleus accumbens in 475 participants. Decreased reward-related effective connectivity from the medial prefrontal cortex to striatum was associated with increased depressive symptom severity in 165 participants. Decreased striatal activity may have been due to decreased cortical to striatal connectivity consistent with glutamatergic and cortical-limbic related theories of depression and resulted in reduced direct pathway basal ganglia output. Further study of basal ganglia pathophysiology is required to better understand these abnormalities in patients with depressive symptoms and syndromes.

Dataset Information

Cognitive control links alcohol use, trait disinhibition, and reduced cognitive capacity: Evidence for medial prefrontal cortex dysregulation during reward-seeking behavior.

Background

Methods

Results

Conclusions

Publications

Cognitive control links alcohol use, trait disinhibition, and reduced cognitive capacity: Evidence for medial prefrontal cortex dysregulation during reward-seeking behavior.

Similar Datasets

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