However, these sociological explanations have largely proven to be an impediment to developing and employing evidence-based treatment strategies derived from our emerging understanding of the core neuropathological mechanisms underlying drug addiction. Many social theories have been proffered to explain the vulnerability to relapse, from lack of moral will power to the need for social acceptance. Food and Drug Administration–approved compound for aiding in the cessation of cigarette smoking is varenicline, which has a relapse rate of approximately 60% after 3 months of treatment ( Cahill et al., 2013). Thus, the primary outcome measure of an effective treatment of addiction is the prevention or reduction of ongoing relapse vulnerability ( Vocci and Ling, 2005), yet current pharmacological and behavioral therapies help only a small percentage of addicts achieve enduring relief from relapse. Fundamentally, the core behavioral pathology of addiction to any substance is the propensity to relapse, even after periods of extended abstinence. Further elucidation of how drugs of abuse alter glutamatergic plasticity within the accumbens will be necessary for the development of new therapeutics for the treatment of addiction across all classes of addictive substances.Ärug addiction is a pervasive neuropsychiatric disease that imposes an immense societal cost. Finally, we examine results from clinical trials in which pharmacotherapies designed to manipulate glutamate systems have been effective in treating relapse in human patients. Then we provide a review of the literature describing how synaptic plasticity in the accumbens is altered after exposure to drugs of abuse and withdrawal and also how pharmacological manipulation of glutamate systems in the accumbens can inhibit drug seeking in the laboratory setting. Next we discuss rodent models of addiction and assess the viability of these models for testing candidate pharmacotherapies for the prevention of relapse. First, we explore the nucleus accumbens, including the cell types and neuronal populations present as well as afferent and efferent connections. In this review, we focus on the role that glutamate signal transduction in the nucleus accumbens plays in addiction-related behaviors. These drug-induced neuroadaptations serve as the molecular basis for relapse vulnerability. A number of alterations in glutamatergic transmission occur within the nucleus accumbens after withdrawal from chronic drug exposure. Chronic exposure to several classes of drugs of abuse disrupts plasticity in this region, allowing drug-associated cues to engender a pathologic motivation for drug seeking. The nucleus accumbens is a major input structure of the basal ganglia and integrates information from cortical and limbic structures to mediate goal-directed behaviors.
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