![]() ![]() Despite these clues, it is not yet fully understood how chronic alcoholism affects dynamic functional connectivity of brain systems while engaged in tasks.Įven minimal disruption of neural connectivity can have a significant impact on the interaction of brain circuits that regulate reward, attention, and executive control ( 7– 8). In alcohol abusers, neuroadaptation of reward circuits interferes with normal functional connectivity between midbrain, striato-thalamic, and prefrontal nodes involved in mediating attention ( 5) and decision making ( 6). The circuits involved in these neuroadaptive changes are anchored in midbrain areas with dopaminergic and glutamatergic projections to cortical and striatal sites: ventral striatum for cue-induced alcohol-seeking ( 1), striato-pallado-thalamic loops for automaticity of behavior ( 2), and prefrontal cortices for attentional selection and executive control of pre-potent responses ( 3– 4). Neuroadaptive changes occur in the brain’s response to chronic alcohol consumption. Degree of microstructural fiber integrity predicted robustness of functional connectivity. By contrast, alcoholics exhibited greater midbrain-orbitofrontal cortical network connectivity than controls. A functional dissociation of brain network connectivity between the groups further showed that controls exhibited greater corticocortical connectivity between middle cingulate, posterior cingulate, and medial prefrontal cortices than alcoholics. Here, in alcoholics, greater deviations from the normal PCC activity correlated with higher amounts of lifetime alcohol consumption. Alcoholics showed the opposite pattern: activation during repetition and deactivation during switching. Also, PCC activity was modulated by executive control demands: activated during response switching and deactivated during response repetition. Posterior cingulum fiber integrity predicted the degree of PCC deactivation in controls but not alcoholics. Despite similar lateral frontoparietal activity and functional connectivity in alcoholics and controls when processing conflict, controls deactivated the posterior cingulate cortex (PCC), whereas alcoholics did not. ![]()
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