In this issue of Neuropsychopharmacology there are nine articles describing important discoveries that advance our understanding of the neurobiology of cocaine addiction. That such a confluence of unsolicited research would appear in a single issue of a major journal is surprising, but even more remarkable is that after perusing this issue's compendium of cocaine-related research it is apparent how thoroughly the study of cocaine addiction infiltrates the field of neurobiology. The growth of research associated with cocaine addiction has been exponential (52 publications in 1978, 768 publications in 2008, PubMed search). Importantly, this research has evolved from work based largely on the behavioral and dopaminergic pharmacology of cocaine into diverse neurobiological mechanisms in areas such as learning and memory, neuroplasticity, and genetic and epigenetic regulation of behavior. This expansion is driven largely by the fact that focusing on dopaminergic reward mechanisms has not yielded an effective therapy for cocaine addiction, and a realization that effective therapies must consider chronic cocaine-induced neuroplasticity that underpins synaptic and circuit efficiency, and fundamental adaptive behavioral processes such as learning. The evolutionary chronology of cocaine research is well manifested in the papers in this issue.

Three of the papers further explore involvement of dopamine transmission in the acute and chronic effects of cocaine. Using a naturally occurring mouse line that lacks a nigrostriatal dopamine system, but appears to fully express mesoaccumbens dopamine neurons, Beeler et al find that in contrast to convention, the nigrostriatal system is critical for both the acute and sensitized locomotor effects of cocaine. The studies by Oleson et al and Beveridge et al examine upregulation of dopamine transporters (DAT) induced by chronic cocaine, the former describing changes in DAT during cocaine use, and the latter makes the surprising discovery using an elegant primate model that the upregulation in DAT is short lived and absent by 90 days of cocaine withdrawal. Together, these papers further catalogue DAT involvement in drug intake and withdrawal.

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