@article{130396,
  keywords = {Animals, Disease Models, Animal, Mice, Mice, Inbred C57BL, Mice, Transgenic, DNA Copy Number Variations, Learning, Neuronal Plasticity, Motor Activity, Electrophysiology, Patch-Clamp Techniques, Synapses, Cerebellum, Purkinje Cells, Autistic Disorder, Blinking},
  author = {Claire Piochon and Alexander Kloth and Giorgio Grasselli and Heather Titley and Hisako Nakayama and Kouichi Hashimoto and Vivian Wan and Dana Simmons and Tahra Eissa and Jin Nakatani and Adriana Cherskov and Taisuke Miyazaki and Masahiko Watanabe and Toru Takumi and Masanobu Kano and Samuel Wang and Christian Hansel},
  title = {Cerebellar plasticity and motor learning deficits in a copy-number variation mouse model of autism},
  abstract = {<p>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.</p>
},
  year = {2014},
  journal = {Nat Commun},
  volume = {5},
  pages = {5586},
  month = {11/2014},
  issn = {2041-1723},
  doi = {10.1038/ncomms6586},
  language = {eng},
}