Dysbindin deficiency in sandy mice causes reduction of snapin and displays behaviors related to schizophrenia

doi:10.1016/j.schres.2008.07.018

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	Dysbindin deficiency in sandy mice causes reduction of snapin and displays behaviors related to schizophrenia
	Feng, Ya-Qin 1,3; Zhou, Zhi-Yong 3; He, Xin 3; Wang, Hao 1,3; Guo, Xiao-Li 1,3; Hao, Chan-Juan 1,3; Guo, Yang 2; Zhen, Xue-Chu 2; Li, Wei 3
刊名	SCHIZOPHRENIA RESEARCH
	2008-12
卷号	106 期号:2-3 页码:218-228
关键词	Schizophrenia Behavior Dysbindin Snapin Synaptic transmission
ISSN号	0920-9964
DOI	10.1016/j.schres.2008.07.018
文献子类	Article
英文摘要	Schizophrenia (SCZ) is a complex trait with a high heritability. The DTNBP1 gene (encoding dysbindin) is one of the leading susceptible genes of SCZ. This risk gene has been reported to be associated with clinical symptoms such as negative symptoms and cognitive deficits. Although reduction of dysbindin expression in schizophrenic brain tissue has been reported, how this contributes to its symptomatology remains uncertain. The sandy (sdy) mouse, which harbors a spontaneously occurring deletion in the Dtnbp1 gene and expresses no dysbindin protein, provides a unique tool to study the role of dysbindin in SCZ. Our recent findings reveal that the sdy mice exhibit specific defects of neurosecretion and synaptic morphology in hippocampal neurons. We here further described that sdy manifested schizophrenia-like behaviors such as social withdrawal and cognitive deficits. In sdy hippocampus, the steady-state level of snapin (a SNAP25-binding protein and a synaptic priming regulator) was reduced due to loss of dysbindin. We further characterized that a 30-residue peptide in dysbindin (90-119 amino acids) mediated the interaction with snapin. Our results suggest that the destabilization of snapin in sdy mice may lead to abnormal neurotransmission and therefore abnormal behaviors. This further defines the sdy mutant as a potential model in schizophrenia research. (C) 2008 Elsevier B.V. All rights reserved.
WOS关键词	LYSOSOME-RELATED ORGANELLES ; HIPPOCAMPAL-FORMATION ; SUSCEPTIBILITY GENE ; 6P22.3 GENE ; DTNBP1 ; BIOGENESIS ; PROTEIN ; ASSOCIATION ; BLOC-1 ; BRAIN
WOS研究方向	Psychiatry
语种	英语
出版者	ELSEVIER SCIENCE BV
WOS记录号	WOS:000261850300015
内容类型	期刊论文
源URL	[http://119.78.100.183/handle/2S10ELR8/279424]
专题	药理学第二研究室
通讯作者	Li, Wei
作者单位	1.Chinese Acad Sci, Grad Sch, Beijing 100039, Peoples R China 2.Chinese Acad Sci, Shanghai Inst Mat Med, Shanghai 200031, Peoples R China; 3.Chinese Acad Sci, Inst Genet & Dev Biol, Key Lab Mol & Dev Biol, Beijing 100101, Peoples R China;
推荐引用方式 GB/T 7714	Feng, Ya-Qin,Zhou, Zhi-Yong,He, Xin,et al. Dysbindin deficiency in sandy mice causes reduction of snapin and displays behaviors related to schizophrenia[J]. SCHIZOPHRENIA RESEARCH,2008,106(2-3):218-228.
APA	Feng, Ya-Qin.,Zhou, Zhi-Yong.,He, Xin.,Wang, Hao.,Guo, Xiao-Li.,...&Li, Wei.(2008).Dysbindin deficiency in sandy mice causes reduction of snapin and displays behaviors related to schizophrenia.SCHIZOPHRENIA RESEARCH,106(2-3),218-228.
MLA	Feng, Ya-Qin,et al."Dysbindin deficiency in sandy mice causes reduction of snapin and displays behaviors related to schizophrenia".SCHIZOPHRENIA RESEARCH 106.2-3(2008):218-228.