Innate social behaviors, such as mating and fighting, are fundamental to animal reproduction and survival. However, social engagements can also put an individual at risk. Little is known about the neural mechanisms that allow for appropriate risk assessment and the suppression of hazardous social interactions. We have identified the posteromedial nucleus of the cortical amygdala (COApm) as a locus required for the suppression of male mating when a female is sick. Using anatomical tracing, functional imaging, and circuit-level epistatic analyses, we show that suppression of mating with an unhealthy female is mediated by the COApm projections onto the glutamatergic population of the medial amygdalar nucleus (MEA). We further show that the role of the COApm to MEA connection in regulating male mating behavior relies on the neuromodulator thyrotropin-releasing hormone (TRH). TRH is expressed in the COApm while

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The ability to encode and update information about individuals is critical for lasting social relationships. Although the hippocampus is important for social recognition memory, its underlying neural representations remain elusive. Here we investigate the neural codes mediating social recognition and learning by examining social odor recognition and associative odor-reward learning in mice. We performed high-resolution calcium imaging from the hippocampal CA2 region of awake head-fixed mice, as CA2 is necessary for social recognition memory. We find that CA2 encodes specific neural representations of novel social odors that are further refined during associative odor-reward learning. Optogenetic silencing of CA2 impairs the formation of reward associations. Furthermore, CA2 population activity represents odors in a geometry that enables abstract representations of social versus non-social odors. Thus, CA2 distinguishes multiple forms of olfactory stimuli to enhance the learning of social odors and associations, which are poised to serve as substrates of social memory.