Prefrontal Cortex and Social Cognition in Mouse and Man.

Schahram Akbarian,Hirofumi Morishita,Hiroyuki Koike,Lucy K. Bicks

doi:10.3389/fpsyg.2015.01805

Abstract

Social cognition is a complex process that requires the integration of a wide variety of behaviors, including salience, reward-seeking, motivation, knowledge of self and others, and flexibly adjusting behavior in social groups. Not surprisingly, social cognition represents a sensitive domain commonly disrupted in the pathology of a variety of psychiatric disorders including Autism Spectrum Disorder (ASD) and Schizophrenia (SCZ). Here, we discuss convergent research from animal models to human disease that implicates the prefrontal cortex (PFC) as a key regulator in social cognition, suggesting that disruptions in prefrontal microcircuitry play an essential role in the pathophysiology of psychiatric disorders with shared social deficits. We take a translational perspective of social cognition, and review three key behaviors that are essential to normal social processing in rodents and humans, including social motivation, social recognition, and dominance hierarchy. A shared prefrontal circuitry may underlie these behaviors. Social cognition deficits in animal models of neurodevelopmental disorders like ASD and SCZ have been linked to an altered balance of excitation and inhibition (E/I ratio) within the cortex generally, and PFC specifically. A clear picture of the mechanisms by which altered E/I ratio in the PFC might lead to disruptions of social cognition across a variety of behaviors is not well understood. Future studies should explore how disrupted developmental trajectory of prefrontal microcircuitry could lead to altered E/I balance and subsequent deficits in the social domain.

Highlights

Social behavior deficits are a fundamental dimension of many psychiatric disorders including the neuordevelopmental disorders Autism Spectrum Disorder (ASD) and SCZ, yet much remains to be learned about the underlying pathophysiology of these deficits
We focus on three major facets of social cognition: social motivation, knowledge of self and other, and group dynamics, because these aspects of social behavior have shown relevance to psychiatric disorders, in humans and in translational animal models (Figure 1)
Tests of the NMDAR hypothesis of SCZ have revealed the importance of NMDAR functioning and intact E/I balance in social recognition, yet no study has pointed to disrupted E/I balance within the prefrontal cortex (PFC) as causally disrupting social recognition

Summary

Introduction

Social behavior deficits are a fundamental dimension of many psychiatric disorders including the neuordevelopmental disorders ASD and SCZ, yet much remains to be learned about the underlying pathophysiology of these deficits. We focus on three major facets of social cognition: social motivation, knowledge of self and other, and group dynamics, because these aspects of social behavior have shown relevance to psychiatric disorders, in humans and in translational animal models (Figure 1). Social behaviors requiring knowledge of self and other are consistently related to activation within the PFC, and in particular a medial region of the PFC that includes the mPFC and the dmPFC (Amodio and Frith, 2006) (Figure 1).

Results

Conclusion