| Social experience has a profound influence on communication across species. In part, this is due to the reorganization of neurochemical systems in the brain that regulate communication behavior, including the serotonergic system. The serotonergic system plays a key role in the brain's response to social context, and through its extensive projections, it can potentially coordinate neural states across regions, including those involved in communication. Here, I explore how social experience influences the neuromodulator serotonin as a mechanism for linking auditory processing with social context. In my first aim, I demonstrate that socially induced elevations in serotonergic activity are triggered by social partners, and the degree of serotonergic elevation corresponds to variation in social behavior. For aims two through four, I focus on how early-life social experience affects both signals and signal receivers by housing animals in groups or in isolation. In aim two, I demonstrate that social isolation alters the expression of vocal signals during male-male encounters, finding that group-housed males emit more stereotyped vocalizations compared to isolated males. In my third aim, I demonstrate that isolated animals exhibit a delayed elevation in socially induced serotonergic activity in an auditory midbrain region, compared with group-housed animals. Further, social isolation abolishes relationships between serotonin and behavior, whereas group-housed animals demonstrate previously described serotonin-behavior relationships. Finally, in my fourth aim, I demonstrate that the effects of social isolation on socially induced serotonergic activity are not due to changes in serotonergic fiber density in the auditory midbrain. Taken together, my findings demonstrate that social isolation alters the context-dependent regulation of sensory processing by one of the brain's major social systems, and contribute to the idea that social isolation in early life interferes with the development of social competence. |
