Modeling schizophrenia in neuregulin 1 and ErbB4 mutant mice

Yisheng Lu; Dong Min Yin; Wen Cheng Xiong; Lin Mei

doi:10.1007/978-1-61779-157-4_12

Modeling schizophrenia in neuregulin 1 and ErbB4 mutant mice

Yisheng Lu
, Dong Min Yin
, Wen Cheng Xiong
, Lin Mei^*

^*Corresponding author for this work

Institute of Molecular Medicine and Genetics and Department of Neurology
Augusta University

Research output: Chapter in Book/Report/Conference proceeding › Chapter › peer-review

2 Scopus citations

Abstract

Schizophrenia, a most prevalent brain disorder, remains to be one of the least understood. Unlike Alzheimer's disease or Parkinson's disease, schizophrenia lacks clear pathological lesions, which has made it difficult to model in animals. However, genetic studies have recently identified many susceptibility genes of this disorder including neuregulin 1 (NRG1) and its receptor ErbB4. Arguably, relevant mutant mice have provided a unique opportunity to model "schizophrenia" in animals where expression or function of susceptibility genes is altered. This review summarizes recent studies of NRG1 and ErbB4 mutant mice and their implication in schizophrenic pathology.

Original language	English
Title of host publication	Animal Models of Schizophrenia and Related Disorders
Editors	Patrick O'Donnell
Pages	261-277
Number of pages	17
DOIs	https://doi.org/10.1007/978-1-61779-157-4_12
State	Published - 2011
Externally published	Yes

Publication series

Name	Neuromethods
Volume	59
ISSN (Print)	0893-2336
ISSN (Electronic)	1940-6045

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

Keywords

ErbB4
Neuregulin 1
hyperactivity
mouse model
neurotransmission
prepulse inhibition
psychiatric disorders
rodents
schizophrenia
synaptic plasticity
working memory

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10.1007/978-1-61779-157-4_12

Cite this

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KW - neurotransmission

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KW - synaptic plasticity

KW - working memory

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Modeling schizophrenia in neuregulin 1 and ErbB4 mutant mice

Abstract

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UN SDGs

Keywords

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