Neural regulation of the time course for cocaine-cue extinction consolidation in rats.

Sites within the hippocampus, amygdala and prefrontal cortex may regulate how responses maintained by cues associated with cocaine are extinguished. To test the role of various brain sites in the consolidation of cocaine-cue extinction learning, the dorsal subiculum (dSUB), rostral basolateral amygdala (rBLA) and infralimbic prefrontal cortex (IL) were manipulated in rats. Following cocaine self-administration training (cues present, cocaine available), responding was assessed during 1-h extinction tests (cues present, no cocaine available).

Involvement of the dorsal subiculum and rostral basolateral amygdala in cocaine cue extinction learning in rats.

Memory system circuitry may regulate how cues associated with cocaine are extinguished, and understanding neurosubstrates of extinction may lead to the development of improved treatment strategies for cocaine addiction. Sites within the hippocampus and amygdala were investigated for their role in regulating cocaine cue extinction learning. Initially, rats were trained to self-administer cocaine under a second-order reinforcement schedule (cocaine and cocaine cues present) followed by a 2-week abstinence period.

D-cycloserine deters reacquisition of cocaine self-administration by augmenting extinction learning.

Augmentation of cue exposure (extinction) therapy with cognitive-enhancing pharmacotherapy may offer an effective strategy to combat cocaine relapse. To investigate this possibility at the preclinical level, rats and squirrel monkeys were trained to self-administer cocaine paired with a brief visual cue. Lever pressing was subsequently extinguished by withholding cocaine injections while maintaining response-contingent presentations of the cue.