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Indirect evidence supports a link between disrupted serotonin (5-hydroxytryptamine 5-HT) signaling in the brain and addictive behaviors. Modified with permission from Volkow et al. MPH was administered IV at the following doses (in mg/kg): 0.5 (circles), 0.25 (squares), 0.1 (diamonds), and 0.025 (triangles). Measurements are done first after injection of a placebo and then, after drug administration, such that the difference in raclopride (positron) signal between the two conditions can be used to estimate the amount of receptor occupancy and, thus, the magnitude of any drug-induced DA increase. PET studies are carried out with a radiolabeled compound such as raclopride that binds to dopamine receptors (D2R) whenever they are not occupied by DA. Regression lines for the correlation between MPH-induced changes in D2R availability in striatum and MPH-induced changes in self-reports of high (r = 0.78, df22, p < 0.0001). B: MPH significantly increased ratings of high. MPH-reduced binding of raclopride dose-dependently in the striatum, where it competes with DA for binding to DA D2 receptors (D2R).
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Stimulant-dependent DA increases in the striatum are associated with the feeling of “high.” A: Distribution volume (DV) images of raclopride for one of the subjects at baseline and after administration of 0.025 and 0.1 mg/kg i.v. Upon exposure to the drug, drug cues or stress this results in unrestrained hyperactivation of the motivation/drive circuit that results in the compulsive drug intake that characterizes addiction. The ability of addictive drugs to co-opt neurotransmitter signals between neurons (including dopamine, glutamate, and GABA) modifies the function of different neuronal circuits, which begin to falter at different stages of an addiction trajectory.
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Although initial experimentation with a drug of abuse is largely a voluntary behavior, continued drug use can eventually impair neuronal circuits in the brain that are involved in free will, turning drug use into an automatic compulsive behavior. The dysfunctions reflect (a) decreased sensitivity of reward circuits, (b) enhanced sensitivity of memory circuits to conditioned expectations to drugs and drug cues, stress reactivity, and (c) negative mood, and a weakened control circuit. Based on brain imaging findings, we present a model according to which addiction emerges as an imbalance in the information processing and integration among various brain circuits and functions.