Addiction, including alcohol use disorder, is a maladaptive form of learning and memory. Initially, the effects of an addictive substance are rewarding, reinforcing the drug-seeking behavior. Over time, repeated exposure leads to changes in neuroanatomy, altering the brain’s circuitry and resulting in cycles of drug binge, withdrawal, and craving, undermining the individual’s health and functioning. This dissertation aims to examine the role of Rac1 in maladaptive learning and Prosapip1 in normal learning and memory. The first chapter examines a protein that has not previously been studied in mammals in the context of AUD, Rac1. In this chapter, we present evidence that Rac1 is activated in the DMS in response to repeated cycles of alcohol binge and withdrawal. This subregion-specific activation leads to phosphorylation of downstream proteins and promotes F-actin assembly, which then causes increased dendritic arborization and dendritic spine maturation. We also show that Rac1 in the DMS is involved in alcohol-associated goal-directed behavior, and therefore likely contributing to the progression of AUD. The second chapter investigates the physiological role of a protein previously associated with AUD, Prosapip1. We developed a Prosapip1 neuronal knockout mouse line to examine its mechanism of action in vivo. We present data to suggest that Prosapip1 is vital in regulating the PSD scaffold. Disruption of the PSD leads to a loss of LTP. Finally, these biomolecular changes result in a spatial learning and memory deficit, which is localized to the dorsal hippocampus. In summary, this dissertation contributes to the knowledge of molecular mechanisms controlling normal and maladaptive learning, and identifies potential targets for the treatment of AUD.