Focus on: Neuroscience and treatment: the potential of neuroscience to inform treatment

Abstract

In the 40 years since the founding of the National Institute on Alcohol Abuse and Alcoholism (NIAAA), researchers have gained a better understanding of the brain circuits and brain chemical (i.e., neurotransmitter) systems involved in the development and maintenance of alcoholism and other drug dependence. This understanding has led to the identification of numerous potential targets for pharmacotherapy of addiction. For example, insight into the roles of signaling molecules called endogenous opioids and the neurotransmitter glutamate were fundamental for developing two medications--naltrexone and acamprosate--now used in the treatment of alcoholism. However, the processes of dependence development (e.g., reinforcement, sensitization, and withdrawal) are highly complex and involve a plethora of contributing influences, which also may differ from patient to patient. Therefore, existing pharmacotherapies still are effective only for some but not all alcoholic patients. Accordingly, researchers are continuing to explore the processes involved in addiction development to identify new targets for treatment and develop new medications that can address different aspects of the dependence syndrome, thereby increasing the likelihood of successful treatment. NIAAA continues to play a pivotal role in funding and conducting this research in order to provide effective treatment options to millions of alcohol-dependent patients.

Figure

Neurocircuitry schematic illustrating the combination of neuroadaptations in the brain circuitry for the three stages of the addiction cycle that drive drug-seeking behavior in the addicted state. Note the activation of the ventral striatum/dorsal striatum in the binge intoxication stage. During the withdrawal–negative-affect stage, the dopamine systems are compromised and brain stress systems such as CRF are activated to reset further the salience of drugs and drug-related stimuli in the context of an aversive dysphoric state. During the preoccupation–anticipation stage, contextual cues via the hippocampus and stimuli cues via the basolateral amygdala converge with frontal cortex activity to drive drug seeking. Other components in the frontal cortex are compromised, producing deficits in executive function. SOURCE: Koob et al. 2008.