During my time in the Szumlinski Lab at UCSB I played a major role as a research assistant for a cocaine self-administration project. This project tested how glutamate-altering drugs microinfused into the prelimbic (PL) and infralimbic (IL) cortices impacted cue-elicited drug seeking following protracted withdrawal from long access cocaine I.V. self-administration. Following a 10-day course of cocaine self-administration, cocaine access was removed for 3 or 30 days until the cue-test day. Animals received bilateral infusions targeting the IL or PL (0.5 μl/side) with the mGlu2/3 agonist LY379268 to lower endogenous glutamate, or the excitatory amino acid transporter inhibitor threo-β-benzyloxyaspartate (TBOA) to raise endogenous glutamate. Following infusion, they were given a 30-min test for cue-reinforced drug-seeking. As discussed in Shin et al. 2018, Vehicle-infused rats exhibited incubated responding on the cocaine-associated lever. Neither LY379268 nor TBOA altered behavior at 3 days withdrawal, indicating that glutamate within neither sub-region regulates cue-reinforced drug-seeking during early withdrawal. At 30 days withdrawal, intra-PL LY379268 microinjection significantly decreased drug-seeking behavior, while the effect was more modest when infused intra-IL. Interestingly, intra-IL TBOA attenuated incubated drug-seeking during protracted withdrawal, but did not affect behavior when infused intra-PL. These results argue that glutamate release within the PL in response to drug-seeking likely drives the manifestation of incubated cocaine-seeking during protracted withdrawal. My responsibilities included executing the behavioral work, assisting with tissue collection and histology, and site-specific pharmacology (microinjections).