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Shank3 mutant mice display autistic-like behaviours and striatal dysfunction

机译：Shank3突变小鼠表现出自闭症样行为和纹状体功能障碍

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摘要

Autism spectrum disorders (ASDs) comprise a range of disorders that share a core of neurobehavioural deficits characterized by widespread abnormalities in social interactions, deficits in communication as well as restricted interests and repetitive behaviours. The neurological basis and circuitry mechanisms underlying these abnormal behaviours are poorly understood. SHANK3 is a postsynaptic protein, whose disruption at the genetic level is thought to be responsible for the development of 22ql3 deletion syndrome (Phelan-McDermid syndrome) and other non-syndromic ASDs. Here we show that mice with Shank3 gene deletions exhibit self-injurious repetitive grooming and deficits in social interaction. Cellular, electrophysiological and biochemical analyses uncovered defects at striatal synapses and corn'co-striatal circuits in Shank3 mutant mice. Our findings demonstrate a critical role for SHANK3 in the normal development of neuronal connectivity and establish causality between a disruption in the Shank3 gene and the genesis of autistic-like behaviours in mice.
机译：自闭症谱系障碍（ASD）包括一系列共享神经行为缺陷核心的疾病，其特征是广泛的社交互动异常，沟通缺陷以及有限的兴趣和重复性行为。这些异常行为的神经基础和电路机制了解甚少。 SHANK3是一种突触后蛋白，其在基因水平上的破坏被认为是22ql3缺失综合征（Phelan-McDermid综合征）和其他非综合征性ASD发生的原因。在这里，我们显示具有Shank3基因缺失的小鼠表现出自我伤害性的重复修饰和社交互动中的缺陷。细胞，电生理和生化分析发现了Shank3突变小鼠的纹状体突触和玉米共纹状体回路中的缺陷。我们的发现表明，SHANK3在神经元连接的正常发育中起关键作用，并在Shank3基因的破坏与小鼠自闭症行为的发生之间建立因果关系。

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  • 来源
    《Nature》 |2011年第7344期|p.437-442|共6页
  • 作者

    Joao Peca; Catia Feliciano; Jonathan T. Ting; Wenting Wang; Michael F. Wells; Talaignair N. Venkatraman; Christopher D. Lascola; Zhanyan Fu; Guoping Feng;

  • 作者单位

    Department of Neurobiology, Duke University Medical Center, Durham, North Carolina 27710, USA,PhD Programme in Biomedicine and Experimental Biology (BEB), Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal;

    Department of Neurobiology, Duke University Medical Center, Durham, North Carolina 27710, USA,Gulbenkian PhD Programme in Biomedicine, Gulbenkian Science Institute, 2781-901 Oeiras, Portugal;

    Department of Neurobiology, Duke University Medical Center, Durham, North Carolina 27710, USA;

    Department of Neurobiology, Duke University Medical Center, Durham, North Carolina 27710, USA;

    Department of Neurobiology, Duke University Medical Center, Durham, North Carolina 27710, USA;

    Department of Radiology, and Brain Imaging and Analysis Center, Duke University Medical Center, Durham, North Carolina 27710, USA;

    Department of Neurobiology, Duke University Medical Center, Durham, North Carolina 27710, USA,Department of Radiology, and Brain Imaging and Analysis Center, Duke University Medical Center, Durham, North Carolina 27710, USA;

    Department of Neurobiology, Duke University Medical Center, Durham, North Carolina 27710, USA,Department of Psychiatry and Behavioral Science, Duke University Medical Center, Durham, North Carolina 27710, USA,McGovem Institute for Brain Research, Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA;

    Department of Neurobiology, Duke University Medical Center, Durham, North Carolina 27710, USA,McGovem Institute for Brain Research, Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA,Stanley Center for Psychiatric Research, Broad Institute, Cambridge, Massachusetts 02142, USA;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
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