Jordan Scheunemann

The opioid epidemic in the United States has grown over the last two decades taking countless lives and steps must be taken to further understand the neurological mechanisms behind addiction (Manchikanti et al, 2010). In opioid withdrawal, negative symptoms have adverse effects on brain function leading to increased vulnerability to relapse in drug use (Koob and Volkow, 2016). In this experiment heat shock transcription factor 1(HSF1) is looked at as a possible regulator for opioid withdrawal as it regulates heat shock proteins in the nucleus accumbens, which is indicated in the reward-circuitry of the brain commonly studied in addiction (Hikida et al, 2013). In previous literature it was found that some behavioral responses to opioid exposure such as psychomotor sensitization and withdrawal are regulated by these heat shock proteins (Wang et al, 2013). Using mice that have had the HSF1 gene knocked down (HSF1 KD) a locomotor activity test was run while inducing repeated opioid withdrawal over several days to determine the effect of HSF1 on opioid withdrawal induced behavior. When HSF1 is downregulated, we would expect to see attenuation in psychomotor sensitization after experiencing repeated cycles of withdrawal. This new understanding of the HSF1 gene and its role in opioid withdrawal behavior could be crucial in advancing treatments for chronic morphine and opioid addiction.