Emmanuel Ikebude

Cocaine, a well known stimulant that blocks the reuptake of dopamine in the synapse, is known to alter structural plasticity in the brain, such as with synaptic strength in the nucleus accumbens (NAc), which is one of the key brain regions found to be involved in the modulation of the dopamine reward pathway. Two synaptic adhesion molecules (SAMs) that are found in the synaptic membranes of the NAc, and all other brain regions are neurexins (NRXNs) and neuroligins (NLGNs). These proteins together support and regulate the synaptic cleft between presynaptic and postsynaptic neurons respectively. Numerous studies have shown how the use of alcohol and opioids change the properties, functions, and levels of NRXNs and NLGNs. However, even with all this research about the effects of cocaine and the function of these SAMs, there is little knowledge on how cocaine specifically may impact their genetic or proteomic expression. In this study, we investigated the impact of cocaine sensitization on those two SAMs in the NAc shell (NAcS), NAc core (NAcC), and other brain regions adjacent the dopamine reward pathway. We hypothesized that cocaine sensitization would end up increasing the level of these SAMs compared to controls treated with no cocaine. For this experiment, male and female rats were administered a baseline intraperitoneal (IP) injection on day 1, then randomized into treatment or control groups. On days 2-8, the treatment and control groups received an IP injection of cocaine (treatment, 15 mg/kg) or saline (control) once each day. Samples from the NAcS, NAcC, and dSTr were assessed through the use of western blotting and quantitative RNA analysis. After, statistical processing was done to find where effects were lain in the treatment of rats with cocaine versus rats with saline, along with other comparisons such as sex and sensitization.