Effects of Nicotine and Conventional Anxiolytics in Male and Female Mice Lacking of Regulator of G-protein Signaling 2 and Their Wildtype Counterparts

Over 42.1 millions of Americans nowadays smoke regularly, and such tobacco use plays an important role in nicotine dependence. A high percentage of smokers suffer from emotional issues such as anxiety and depression. In fact, nicotine can induce anxiolytic effects. In humans, polymorphisms of regulator of G-protein signaling 2 (RGS2), which suggest decreased functioning of RGS2, are associated with anxiety. RGS2 proteins negatively regulate intracellular signaling pathways for neurotransmitters like serotonin that play an important role in mediating anxiety. However, the anxiolytics effects of nicotine and conventional anxiolytics in mice lacking RGS2 have not been evaluated. Thus, the objective of the research was to determine the role of the RGS 2 proteins and sex (male vs. female) in anxiolytic effects of nicotine and conventional anxiolytics such as fluoxetine and desipramine. The hypothesis of this project is that mice lacking RGS 2 protein are more sensitive compared to wildtype mice to the anxiolytic effects of nicotine. Further, we hypothesize that mice lacking RGS2 will be more sensitive to anxiolytic effects of fluoxetine and desipramine, but not bupropion. The data are being analyzed. If the data are as hypothesized, it will suggest a role for RGS2 in both anxiety and nicotine addiction.