Rapid, transient synaptic plasticity in addiction

• Glutamatergic input to the nucleus accumbens and its involvement in drug relapse is discussed.
• Cue-induced relapse to cocaine requires rapid, transient plasticity in accumbens.
• Future directions for relapse prevention are discussed.

Chronic use of addictive drugs produces enduring neuroadaptations in the corticostriatal glutamatergic brain circuitry. The nucleus accumbens (NAc), which integrates cortical information and regulates goal-directed behavior, undergoes long-term morphological and electrophysiological changes that may underlie the increased susceptibility for relapse in drug-experienced individuals even after long periods of withdrawal. Additionally, it has recently been shown that exposure to cues associated with drug use elicits rapid and transient morphological and electrophysiological changes in glutamatergic synapses in the NAc. This review highlights these dynamic drug-induced changes in this pathway that are specific to a drug seeking neuropathology, as well as how these changes impair normal information processing and thereby contribute to the uncontrollable motivation to relapse. Future directions for relapse prevention and pharmacotherapeutic targeting of the rapid, transient synaptic plasticity in relapse are discussed.This article is part of a Special Issue entitled ‘NIDA 40th Anniversary Issue’.