Myjak, Julia E2018-04-172018-04-172018https://hdl.handle.net/11299/195767Alcohol and nicotine addiction are often co-morbid with no single drug currently available to treat both conditions. Protein kinase C epsilon (PKCε) is known to act upon the neuronal nicotinic acetylcholine receptors (nAChRs), which are involved in the mechanisms of alcohol and nicotine addiction. All current approved therapies for nicotine addiction target the nAChRs. Previous studies have shown that male mice with a genetic deletion of the PKCε gene (knockout mice) have reduced nicotine consumption compared to wild-types. The consumption of nicotine in female mice has not yet been tested. In this study, we evaluated nicotine consumption of in PKCε knockout and wild-type female mice using a voluntary oral consumption procedure. Our voluntary oral consumption method is a better representation of human consumption compared to investigator- administered nicotine. Mice underwent a two-bottle choice experiment with access to nicotine in 2% saccharin solution and a 2% saccharin solution for four weeks. The concentration of nicotine did not change over the four weeks. We found there was a genotype difference when compared with the previous results in males. Female PKCε knock-out mice consumed more nicotine compared with wild-type mice in the first week. Thereafter, female PKCε knock-out mice had similar nicotine consumption compared with wild-type mice. Our results indicate that a sex by genotype difference exists in the contribution of PKCε to nicotine consumption. These experimental results contribute further knowledge of the role of PKCε in nicotine consumption and may play a role in future development of treatment options for nicotine addiction.enPresentation