title: Optogenetic insights into social behavior function.
abstract: Cognitive and social deficits lie at the core of many neuropsychiatric diseases and are among the many behavioral symptoms not amenable to pharmacological intervention. Despite significant advances in identifying genes potentially involved in the pathogenesis of complex psychiatric conditions such as autism and schizophrenia, knowledge of the physiological functions that are affected (and are therefore potential targets for clinical intervention) is scarce. In psychiatric disorders with a strong genetic component, animal models have provided important links between disease-related genes and behavioral impairment. Social dysfunction, for instance, is commonly observed in transgenic rodent disease models. However, the causal relationships between the behavioral and physiological abnormalities in these models are not well-understood. Optogenetic techniques have evolved to provide a wide range of experimental paradigms in which neural circuit activity can be perturbed with high spatial and temporal precision, enabling causal investigation of the function of defined physiological events in neuronal subgroups. With optogenetics, researchers have begun to elucidate the basic neural mechanisms of social behaviors and of disease-relevant social and cognitive dysfunction. The synthesis of optogenetic technology with genetic animal models will allow forward- and reverse-engineering approaches to investigating the neural correlates of psychiatric disease. This review outlines the neural systems known to be involved in social behavior, illustrates how optogenetic technology has been applied to analyze this circuitry, and imagines how it might be further developed in future studies to elucidate these complex circuits both from a basic science perspective and in the context of psychiatric disease.
authors.affiliation: Department of Neurobiology, Weizmann Institute of Science, Rehovot, Israel. ofer.yizhar@weizmann.ac.il
authors.forename: Ofer
authors.initials: O
authors.lastname: Yizhar
mesh_terms: D000818:Animals; D001321:Autistic Disorder / Q000209:etiology / Q000503:physiopathology; D003072:Cognition Disorders / Q000503:physiopathology*; D018390:Gene Targeting / Q000379:methods*; D006801:Humans; D001523:Mental Disorders / Q000503:physiopathology*; D009474:Neurons / Q000502:physiology*; D055355:Opsins / Q000235:genetics; D010775:Photic Stimulation / Q000379:methods*; D017397:Prefrontal Cortex / Q000503:physiopathology*; D012559:Schizophrenia / Q000209:etiology / Q000503:physiopathology; D012919:Social Behavior
chemical_list: D055355:Opsins