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Alcoholism is a debilitating neuropsychiatric disorder that adversely affects many people worldwide. Understanding the neurobiological mechanisms that cause alcohol addiction is paramount to its treatment. New evidence suggests that addictive behaviors emerge as a result of plastic changes in the neural circuitry that mediates drug reinforcement and reward-learning. The goal of this dissertation was to identify changes in neuroplasticity-related proteins following alcohol consumption in areas of the brain that mediate alcohol reward. Initially, we analyzed the amygdala proteome following chronic alcohol consumption and found 26 proteins that showed differential protein expression. Several of these proteins are involved in synaptic plasticity including CaMKII[alpha], a protein kinase that modulates receptor activity and is required for the induction of long-term synaptic plasticity. We further characterized CaMKII expression in the amygdala, and found that it is specifically increased in the central and lateral amygdala following twenty-eight days of alcohol-drinking at the start of the dark cycle when there were no detectable blood alcohol levels. Consistent with CaMKII's role in AMPAR trafficking, we found a concomitant increase in AMPA/NMDA ratio in the central amygdala. We extended these findings by measuring CaMKII expression following operant self-administration and found that phosphorylated CaMKII was increased in the amygdala of alcohol-drinking mice. To determine if increased CaMKII activation played a role in alcohol's reinforcing properties, we infused CaMKII inhibitors into the amygdala prior to self-administration sessions. We found that CaMKII inhibition attenuates alcohol but not sucrose operant self-administration and concluded that CaMKII activity in the amygdala functionally regulates the reinforcing properties of alcohol. Lastly, we developed a mouse protocol for relapse-like behavior and tested the role of ERK1/2, a protein kinase that plays a role in plasticity, in relapse-like behavior. We found that inhibition of ERK1/2 phosphorylation potentiates cue-induced reinstatement of alcohol-seeking and induces sucrose-seeking. Collectively, these experiments demonstrate that inhibiting the activity of protein kinases that are involved in synaptic plasticity can affect alcohol-related behaviors in a reinforcer-specific manner and suggest that modulating these pathways has the potential for pharmacotherapeutic intervention in alcoholics.