Aruldas, RachelBuczek, LauraSade, Spencer2022-05-312022-05-312022-05https://hdl.handle.net/11299/227769Cocaine is an addictive stimulant that targets parts of the corticostriatal reward circuit like the medial prefrontal cortex (mPFC) and nucleus accumbens (NAc). The mPFC communicates with the NAc via glutamatergic projections which regulate reward-seeking behavior. Cocaine self-administration downregulates glutamate transporter 1 (GLT1) gene expression and disrupts this communication. We aimed to determine if cocaine impacts GLT1 protein levels in the mPFC and NAc core. Rats were given cocaine or saline injections for six days and a challenge injection on the seventh day. They were divided into groups based on the initial and challenge injections they received: cocaine & cocaine (c-c), cocaine & saline (c-s), saline & cocaine (s-c), saline & saline (s-s). The locomotion of rats was tracked for forty-five minutes following daily injections. On the seventh day, tissue from the rat’s NAc core (NAcC) and mPFC was extracted. Western Blots were used to quantify GLT-1 levels in the collected tissue. We hypothesized that group c-c would have the lowest GLT1 levels and group s-s would have the highest GLT1 levels as those rats had no cocaine exposure. Our results showed that cocaine sensitization had no impact on GLT1 expression levels in the mPFC and NAcC. These results will inform further research into the impact of cocaine sensitization vs self-administration on proteins in specific regions of the brain.enCocaineSensitizationGlutamate Transporter 1Presentation