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FIGURE 1–4. Key common neurocircuitry elements in drug-seeking behavior of addiction.Three major circuits that underlie addiction can be distilled from the literature. A drug reinforcement circuit (reward and stress) is composed of the extended amygdala, including the central nucleus of the amygdala, the bed nucleus of the stria terminalis, and the transition zone in the shell of the nucleus accumbens. Multiple modulator neurotransmitters are hypothesized, including dopamine and opioid peptides for reward; and corticotropin-releasing factor and norepinephrine for stress. The extended amygdala is hypothesized to mediate integration of rewarding stimuli or stimuli with positive incentive salience and aversive stimuli or stimuli with negative aversive salience. During acute intoxication, valence is weighted on processing rewarding stimuli, and, during the development of dependence, aversive stimuli come to dominate function. A drug- and cue-induced reinstatement (craving) neurocircuit is composed of the prefrontal (anterior cingulate, prelimbic, orbitofrontal) cortex and basolateral amygdala, with a primary role hypothesized for the basolateral amygdala in cue-induced craving and a primary role for the medial prefrontal cortex in drug-induced craving, based on animal studies. Human imaging studies have shown an important role for the orbitofrontal cortex in craving (see text). A drug-seeking circuit (compulsive) circuit is composed of the nucleus accumbens, ventral pallidum, thalamus, and orbitofrontal cortex. The nucleus accumbens has long been hypothesized to have a role in translating motivation to action and forms an interface between the reward functions of the extended amygdala and the motor functions of the ventral striatal–ventral pallidal–thalamic-cortical loops. The striatal-pallidal-thalamic loops reciprocally move from prefrontal cortex to orbitofrontal cortex to motor cortex—ultimately leading to drug-seeking behavior. Note that, for the sake of simplicity, other structures are not included, such as the hippocampus (which presumably mediates context-specific learning, including that associated with drug actions). Also note that dopamine and norepinephrine both have widespread innervation of cortical regions and may modulate function relevant to drug addiction in those structures. CRF = corticotropin-releasing factor; DA = dopamine; -END = -endorphin; ENK = emkephalin; NE = norepinephrine; VTA = ventral tegmental area.Source. Reprinted from Koob GF, Le Moal M: Neurobiology of Addiction. London, Academic Press, 2005. Used with permission.


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