Abstract
Relapse, as it applies to addiction, is described as the resumption or reinstatement of drug-taking behavior after periods of prolonged abstinence. In our January column (Williamson et al., 2013), we described a neurobiological process that influences the occurrence of relapse: the complex interactions of glutamate in the brain via drug-associated cues. However, there is more to the story! Not only do drug-associated cues trigger relapse, but there are two additional components that make a trio of relapse precipitants: small doses of addictive drugs (priming) and stressors. Animal models of these three factors have been demonstrated through carefully designed and replicated experiments that implicate separate mechanisms of operation for each (Stewart, 2000). For individuals who are intent on maintaining recovery from addiction, having an understanding of these relapse precipitants can assist in making decisions to support sobriety. We review these other two components of relapse here. First, we review the nature of priming, followed by a more detailed look at the impact of stress. Priming involves use of small …
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