Circuitry of self-control and its role in reducing addiction

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Circuitry of self-control and its role in reducing addiction Yi-Yuan Tang, Michael I. Posner, Mary K. Rothbart, Nora D. Volkow  Trends in Cognitive Sciences  Volume 19, Issue 8, Pages 439-444 (August 2015) DOI: 10.1016/j.tics.2015.06.007 Copyright © 2015 Elsevier Ltd Terms and Conditions

Figure 1 Reward circuits and pathways of basal ganglia. (A) Key structures and pathways of the reward circuit. Arrows indicate main connections of the reward circuit. Abbreviations: Amy, amygdala; dACC, dorsal anterior cingulate cortex; dPFC, dorsal prefrontal cortex; Hipp, hippocampus; hypo, hypothalamus; LHb, lateral habenula; OFC, orbital frontal cortex; PPT, pedunculopontine nucleus; S, shell, SNc, substantia nigra, pars compacta; STN, subthalamic nucleus; Thal, thalamus; vmPFC, ventral medial prefrontal cortex; VP, ventral pallidum; VTA, ventral tegmental area. Reprinted from [74] with permission from Nature Publishing Group. (B) Direct and indirect pathways of the basal ganglia (BG). The principal input of BG is the striatum, receiving excitatory inputs from most cortical areas. The output nuclei of BG are the internal globus pallidus and substantia nigra reticulate (GPi/SNr), which send processed information to the thalamus to eventually feed back an excitatory projection to the cortex. Within this circuitry there are two pathways: a direct pathway that expresses dopamine D1 receptors and an indirect pathway that expresses D2 receptors. D1 striatal neurons inhibit GPi/SNr cells forming the direct pathway. D2 striatal cells inhibit an intermediate relay, the external globus pallidus (GPe), which ultimately provides inhibition to GPi/SNr. Reprinted from [75]. Trends in Cognitive Sciences 2015 19, 439-444DOI: (10.1016/j.tics.2015.06.007) Copyright © 2015 Elsevier Ltd Terms and Conditions

Figure 2 Brain adaptive circuits in three stages of addiction. Schematic illustrating the combination of neuroadaptations in the brain circuitry for the three stages of the addiction cycle that promote drug-seeking behavior in the addicted state. Note the activation of the ventral striatum/dorsal striatum/extended amygdala, driven by cues through the hippocampus and basolateral amygdala, and by stress through the insula. The frontal cortex system is compromised, producing deficits in executive function and contributing to the incentive salience of drugs compared to natural reinforcers. Dopamine systems are compromised, and brain stress systems such as corticotrophin releasing factor are activated to reset further the salience of drugs and drug-related stimuli in the context of an aversive dysphoric state [59,76]. Adapted, with permission, from [59] and [76] and based on [77]. Trends in Cognitive Sciences 2015 19, 439-444DOI: (10.1016/j.tics.2015.06.007) Copyright © 2015 Elsevier Ltd Terms and Conditions

Figure 3 Self-control networks and addictions. Self-control capacities improve following IBMT (but not RT) through increased ACC/PFC activity and ACC–striatum connectivity, and high self-control helps addiction prevention and treatment (e.g., smoking reduction or quitting). Self-control deficits are associated with decreased ACC/PFC activity and ACC–striatum connectivity, and addiction (gray area). Abbreviations: ACC, anterior cingulate cortex; IBMT; integrative body–mind training; PFC, prefrontal cortex; RT, relaxation training. Trends in Cognitive Sciences 2015 19, 439-444DOI: (10.1016/j.tics.2015.06.007) Copyright © 2015 Elsevier Ltd Terms and Conditions