Alcohol is a potent nervous system depressant that primarily modulates GABAA receptors in the brain. Research has shown significant alterations to brain signaling because of chronic alcohol use, particularly in regions of the brain associated with stress. These regions are similarly sensitive to modulation from another positive modulator of GABAA receptors, neurosteroids. While correlations have been drawn between levels of neurosteroids, expression the enzymes crucial in synthesizing them (particularly the two isoforms of 5α-reductase) and chronic alcohol use, it is still unclear what the consequences of these interactions are and how they drive withdrawal and relapse. I am particularly interested in the molecular, physiological and behavior consequences of a chronic ethanol exposure paradigm and how this is impacted by a novel conditional knockout of 5α-reductase to further understand the role of neurosteroids in mediating the long-term consequences of alcohol exposure.