Cerebellar plasticity and motor learning deficits in a copy-number variation mouse model of autism

Claire Piochon, Alexander D. Kloth, Giorgio Grasselli, Heather K. Titley, Hisako Nakayama, Kouichi Hashimoto, Vivian Wan, Dana H. Simmons, Tahra Eissa, Jin Nakatani, Adriana Cherskov, Taisuke Miyazaki, Masahiko Watanabe, Toru Takumi, Masanobu Kano, Samuel S.-H. Wang and Christian Hansel ()
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Claire Piochon: University of Chicago
Alexander D. Kloth: Princeton University
Giorgio Grasselli: University of Chicago
Heather K. Titley: University of Chicago
Hisako Nakayama: Graduate School of Biomedical and Health Sciences, Hiroshima University
Kouichi Hashimoto: Graduate School of Biomedical and Health Sciences, Hiroshima University
Vivian Wan: University of Chicago
Dana H. Simmons: University of Chicago
Tahra Eissa: University of Chicago
Jin Nakatani: Shiga University of Medical Science
Adriana Cherskov: Princeton University
Taisuke Miyazaki: Hokkaido University Graduate School of Medicine
Masahiko Watanabe: Hokkaido University Graduate School of Medicine
Toru Takumi: RIKEN Brain Science Institute
Masanobu Kano: Graduate School of Medicine, The University of Tokyo
Samuel S.-H. Wang: Princeton University
Christian Hansel: University of Chicago

Nature Communications, 2014, vol. 5, issue 1, 1-13

Abstract: Abstract A common feature of autism spectrum disorder (ASD) is the impairment of motor control and learning, occurring in a majority of children with autism, consistent with perturbation in cerebellar function. Here we report alterations in motor behaviour and cerebellar synaptic plasticity in a mouse model (patDp/+) for the human 15q11-13 duplication, one of the most frequently observed genetic aberrations in autism. These mice show ASD-resembling social behaviour deficits. We find that in patDp/+ mice delay eyeblink conditioning—a form of cerebellum-dependent motor learning—is impaired, and observe deregulation of a putative cellular mechanism for motor learning, long-term depression (LTD) at parallel fibre-Purkinje cell synapses. Moreover, developmental elimination of surplus climbing fibres—a model for activity-dependent synaptic pruning—is impaired. These findings point to deficits in synaptic plasticity and pruning as potential causes for motor problems and abnormal circuit development in autism.

Date: 2014
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DOI: 10.1038/ncomms6586

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