Social interactions can be either rewarding or aversive. In many neuropsychiatric disorders, social pathologies underlie disease etiology. For example, decreased social reward is associated with autism spectrum disorder and social stress is a leading risk factor for mood and anxiety disorders. Social interactions are characterized by their intensity (i.e., salience) and whether they are rewarding or aversive (i.e., valence). The mechanisms underlying the salience and valence of social interactions are not well understood. Social stress is one of the most salient stressors across taxa, but it is unclear how an individual’s social status might impact the rewarding or aversive properties of these interactions. If low social rank reduces social reward, it could contribute to the social anhedonia that is characteristic of many social stress-related neuropsychiatric disorders, and if social dominance increases social reward, it could reduce the symptomology of these disorders. The possibility that social stress reduces social reward is supported by evidence that stress can produce long lasting changes in the neural pathways that process reward and reinforcement of behavior, i.e., the mesolimbic dopamine system (MDS), which includes the ventral tegmental area (VTA) and its dopamine (DA) projections to the nucleus accumbens (NAc). Here, we provide evidence to support that DA neurons in the medial VTA (mVTA) that project to the NAc core primarily signal the salience of both rewarding and aversive social interactions. In contrast, DA neurons in the lateral VTA (lVTA) that project to the NAc shell primarily signal valence, with positive valence increasing activation of this subcircuitry. In this dissertation, I tested the hypothesis that dopamine dynamics (DA neuron activity and release patterns) and receptor subtypes within anatomically specific subcircuits of the MDS code, at least in part, the salience and valence of social interactions. Investigating a novel subcircuitry within the MDS that codes for social reward and aversion in males and females seeks to fill the gap in our understanding of social deficits in neuropsychiatric disorders as well as differences in disease prevalence among men and women.