Abstract
Growth factor Neuregulin 1 (NRG1) plays an essential role in development and organization of the cerebral cortex. NRG1 and its receptors, ERBB3 and ERBB4, have been implicated in genetic susceptibility for schizophrenia. Disease symptoms include asociality and altered social interaction. To investigate the role of NRG1-ERBB signaling in social behavior, mice heterozygous for an Nrg1 null allele (Nrg1+/−), and mice with conditional ablation of Erbb3 or Erbb4 in the central nervous system, were evaluated for sociability and social novelty preference in a three-chambered choice task. Results showed that deficiencies in NRG1 or ERBB3 significantly enhanced sociability. All of the mutant groups demonstrated a lack of social novelty preference, in contrast to their respective wild-type controls. Effects of NRG1, ERBB3, or ERBB4 deficiency on social behavior could not be attributed to general changes in anxiety-like behavior, activity, or loss of olfactory ability. Nrg1+/− pups did not exhibit changes in isolation-induced ultrasonic vocalizations, a measure of emotional reactivity. Overall, these findings provide evidence that social behavior is mediated by NRG1-ERBB signaling.
Highlights
Genome-wide linkage studies, case-control association studies, and functional data have implicated Neuregulin 1 (NRG1) in the etiology of schizophrenia [18, 56, 57]
We investigated whether NRG1- and ERBB- deficient mouse models have alterations in social approach, relevant to symptoms of asociality and impaired social interaction in schizophrenia, as well as autism, fragile X syndrome, and other neurodevelopmental disorders
The present study confirms that NRG1-ERBB signaling plays a role in mouse social behavior
Summary
Genome-wide linkage studies, case-control association studies, and functional data have implicated Neuregulin 1 (NRG1) in the etiology of schizophrenia [18, 56, 57]. NRG1 is known to play critical roles in the development and patterning of the cerebral cortex [1, 2, 13, 15, 35, 51, D. Lee Division of Life and Pharmaceutical Sciences, Ewha Womans University, Seoul, Korea. C. Lai Department of Psychological and Brain Sciences and Program in Neuroscience, Indiana University, Bloomington, IN, USA. H. Troy Ghashghaei Department of Molecular Biomedical Science, North Carolina State University, Raleigh, NC, USA. Threadgill Department of Genetics, University of North Carolina School of Medicine, Chapel Hill, NC, USA
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