Mentors: Julia Dziabis, Staci Bilbo, Ph.D.
Department of Psychology and Neuroscience
Microglia are immune cells of the brain and can be activated through toll-like receptors. When alcohol is consumed in excess, microglia produce inflammatory mediators. Zeroing in on the toll-like receptor adaptor molecule MyD88, our lab’s preliminary studies suggest that reduced microglial MyD88 signaling (dampening of inflammation) increases voluntary ethanol consumption. We hypothesized that the mice with altered microglial MyD88, Cre+, would drink more than the controls (Cre-) over a 6 week period. The Cre+ mice would be more anxious as well as having less cognitive flexibility compared to all other groups. To simulate chronic alcohol consumption, we utilized a drinking in the dark paradigm, where Cre+ and Cre- mice were exposed to alcohol 4 days a week for 6 weeks, and the amount consumed was tracked daily. Afterward, behavioral tests, such as Elevated Plus Maze, Light-Dark Box, and Barnes Maze were conducted when the animals were going through withdrawal. Our findings suggest that inhibiting the microglial MyD88-dependent pathway does not increase drinking in the Cre+ group compared to the controls, but overall females consumed more ethanol than males. Further exploration of the mechanisms underlying microglial inflammatory signaling and their relationship to excess alcohol consumption is an area of interest for future projects.