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Deficient NRG1-ERBB signaling alters social approach: relevance to genetic mouse models of schizophrenia
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 investig...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer US
2009
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3164004/ https://www.ncbi.nlm.nih.gov/pubmed/21547722 http://dx.doi.org/10.1007/s11689-009-9017-8 |
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author | Moy, Sheryl S. Troy Ghashghaei, H. Nonneman, Randal J. Weimer, Jill M. Yokota, Yukako Lee, Daekee Lai, Cary Threadgill, David W. Anton, E. S. |
author_facet | Moy, Sheryl S. Troy Ghashghaei, H. Nonneman, Randal J. Weimer, Jill M. Yokota, Yukako Lee, Daekee Lai, Cary Threadgill, David W. Anton, E. S. |
author_sort | Moy, Sheryl S. |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-3164004 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2009 |
publisher | Springer US |
record_format | MEDLINE/PubMed |
spelling | pubmed-31640042011-10-18 Deficient NRG1-ERBB signaling alters social approach: relevance to genetic mouse models of schizophrenia Moy, Sheryl S. Troy Ghashghaei, H. Nonneman, Randal J. Weimer, Jill M. Yokota, Yukako Lee, Daekee Lai, Cary Threadgill, David W. Anton, E. S. J Neurodev Disord Article 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. Springer US 2009-05-27 2009-12 /pmc/articles/PMC3164004/ /pubmed/21547722 http://dx.doi.org/10.1007/s11689-009-9017-8 Text en © Springer Science+Business Media, LLC 2009 |
spellingShingle | Article Moy, Sheryl S. Troy Ghashghaei, H. Nonneman, Randal J. Weimer, Jill M. Yokota, Yukako Lee, Daekee Lai, Cary Threadgill, David W. Anton, E. S. Deficient NRG1-ERBB signaling alters social approach: relevance to genetic mouse models of schizophrenia |
title | Deficient NRG1-ERBB signaling alters social approach: relevance to genetic mouse models of schizophrenia |
title_full | Deficient NRG1-ERBB signaling alters social approach: relevance to genetic mouse models of schizophrenia |
title_fullStr | Deficient NRG1-ERBB signaling alters social approach: relevance to genetic mouse models of schizophrenia |
title_full_unstemmed | Deficient NRG1-ERBB signaling alters social approach: relevance to genetic mouse models of schizophrenia |
title_short | Deficient NRG1-ERBB signaling alters social approach: relevance to genetic mouse models of schizophrenia |
title_sort | deficient nrg1-erbb signaling alters social approach: relevance to genetic mouse models of schizophrenia |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3164004/ https://www.ncbi.nlm.nih.gov/pubmed/21547722 http://dx.doi.org/10.1007/s11689-009-9017-8 |
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