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These studies have shown how repeated drug use can target key molecules and brain circuits, and eventually disrupt the higher order processes that underlie emotions, cognition and behavior. Indeed, research on addiction has started to uncover the sequence of events and long-lasting sequelae that can result from the persistent abuse of an addictive substance. The last 25 years of neuroscience research have produced evidence that addiction is a disease of the brain, providing a powerful argument for upholding the same standards of medical care to the addicted individual as those that are common to other diseases with a major public impact, like diabetes. 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 neuro-transmitter 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.