Krista McFarland

TL;DR: Dopamine release in the dPFC initiates a dP FC–NAcore–VP series circuit that mediates cocaine-induced drug-seeking behavior, and is demonstrated to be specific to drug-related reinstatement.

TL;DR: Together, these data demonstrate that activation of a glutamatergic projection from the prefrontal cortex to the nucleus accumbens underlies cocaine-primed reinstatement of drug-seeking behavior.

TL;DR: In this paper, the authors showed that repeated cocaine treatment and withdrawal produces changes in brain function thought to be involved in relapse to drug use, and that withdrawal from repeated cocaine increases susceptibility to relapse in part by reducing cystine/glutamate exchange, and restoring exchanger activity prevents cocaine-primed drug seeking.

TL;DR: The proposed convergence of priming stimuli into the glutamatergic projection from anterior cingulate to the accumbens core combined with the changes in glutamate transmission and signaling that accompany repeated psychostimulant administration points to the potential value of pharmacological agents that manipulate glutamate release or postsynaptic glutamate receptor signaling and trafficking in treating primed relapse in addicts.

TL;DR: The role of limbic, cortical, and striatal circuitry in a footshock reinstatement model of relapse to cocaine seeking was evaluated and suggested that footshock activates limbic circuitry in the CEA, which in turn activates a VTA dopamine projection to the PFCd.