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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...

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Autores principales: Moy, Sheryl S., Troy Ghashghaei, H., Nonneman, Randal J., Weimer, Jill M., Yokota, Yukako, Lee, Daekee, Lai, Cary, Threadgill, David W., Anton, E. S.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer US 2009
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.
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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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