Of the innate behaviors, mating and aggression are termed as social for these behaviors are elicited by and directed at another social individual. Innate social behaviors, such as mating and aggression, in rodents are driven by the accessory olfactory circuits. Both of these behaviors need to be tightly regulated to prevent inappropriate social interactions under adverse condition (e.g. in the presence of sick females or predators). While previous studies have mostly focused on elucidating neural pathways driving innate social behaviors, neural circuits and mechanism, by which these behaviors are suppressed under inappropriate conditions are poorly understood. As preliminary results, we are able to show that activation of cortical amygdala posterior medial (CoApm), the major recipient of accessory olfactory information, suppresses male reproductive behaviors. Consistent with this inhibitory function, CoApm activity was enhanced by sick conspecifics that are known to inhibit these social behaviors. Together, our preliminary results suggest that the CoApm might be involved in inhibiting innate social behaviors under unfavorable conditions. We will test this hypothesis by asking 1) if CoApm is required to inhibit male reproductive behavior toward sick females, 2) if CoApm mediates this function via its efferents to medial amygdala (MeA), and 3) whether the CoApm to MeA projection is modulated thyrotropin-releasing hormone (TRH).
Innate social behaviors need to be tightly regulated not only to release them upon detection of sensory stimuli but also to prevent the release under inappropriate conditions. Imbalance between these two processes might lead to various disorders of social behaviors like the social anxiety syndrome. In this application, we propose to take an interdisciplinary approach to identify neural circuits responsible for suppressing social behaviors under unfavorable conditions and examine how these circuits could be modulates by a peptide implicated in social anxiety.