In the past few decades, psychostimulant addiction has become increasingly appreciated as a neuropathological disorder marked by chronic and compulsive relapse episodes during which the drive to seek and use drug cannot be controlled (O’Brien, 1996). This may be due to genetic and socioeconomic conditions combined with pharmacologically-induced effects that, upon continued drug use, favor the execution of rigid, drug-associated behaviors in lieu of more adaptive and flexible responding (Kalivas and Volkow, 2005; Kalivas and O’Brien, 2008; Koob et al., 1998). The persistence of drug-induced alterations in brain function has been hypothesized to exacerbate the recidivistic and compulsive nature of drug addiction (Hyman et al., 2006). Thus, addiction is increasingly regarded as an aberrant form of learning (Hyman and Malenka, 2001; Jones and Bonci, 2005). Efforts to understand the molecular basis of this complex disease must therefore rely upon an integrated understanding of how commonly abused drugs alter the synaptic plasticity, neurophysiology, and behavior of model organisms.
