The overarching research goal in our laboratory is to understand how processing in specific brain circuits works to support natural communication behaviors. We aim to reveal neural mechanisms that allow organisms to detect and recognize familiar individuals, to gather information about their identity and social status, and to select appropriate behaviors. Mice are capable of acquiring detailed profiles on one another from the smells and sounds experienced during their social encounters. These dossiers may include information on a mouse’s sex, genetic identity, reproductive state, levels of distress or sexual interest, or even recently consumed foods, details that are indispensable for survival and mating success. Initially, we are working to understand the neuronal activities and mechanisms in primary sensory brain areas that support these forms of communication.  In the future, we anticipate moving deeper into the brain to ascertain where the sensory data from those regions are collected and integrated into hormonal and electrical signals that promote appropriate behavioral choices.

The scientific benefit of this approach is twofold.  First, we want to identify fundamental principles for how the brain controls complex behavior.  To this end, it is our belief that the nervous system’s function is best interpreted in the context of the behaviors it was evolutionarily designed to perform.  Thus, it is advantageous to use natural behaviors such as intraspecific communication.  Second, impairment of social perception and cognition is a core feature of the autism spectrum disorders (ASD); for example, patients may have difficulty perceiving and interpreting communication gestures such as speech, facial expressions, and ‘body language’.   This broad feature is recapitulated in many mouse models of ASD that carry genetic variants identified in human ASD populations.  Therefore, if we can ascertain the neural circuit substrates of social behavior in normal mice, we can make and test predictions for how the circuitry is affected in the mouse models.  The results are likely to tell us more about the synaptic modifications that occur in human autism.