Autistic-like behaviour and cerebellar dysfunction in Purkinje cell Tsc1 mutant mice

Peter T. Tsai (), Court Hull, YunXiang Chu, Emily Greene-Colozzi, Abbey R. Sadowski, Jarrett M. Leech, Jason Steinberg, Jacqueline N. Crawley, Wade G. Regehr and Mustafa Sahin ()
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Peter T. Tsai: The F.M. Kirby Neurobiology Center, Boston Children’s Hospital, Harvard Medical School
Court Hull: Harvard Medical School
YunXiang Chu: Harvard Medical School
Emily Greene-Colozzi: The F.M. Kirby Neurobiology Center, Boston Children’s Hospital, Harvard Medical School
Abbey R. Sadowski: The F.M. Kirby Neurobiology Center, Boston Children’s Hospital, Harvard Medical School
Jarrett M. Leech: The F.M. Kirby Neurobiology Center, Boston Children’s Hospital, Harvard Medical School
Jason Steinberg: The F.M. Kirby Neurobiology Center, Boston Children’s Hospital, Harvard Medical School
Jacqueline N. Crawley: Laboratory of Behavioral Neuroscience, Intramural Research Program, National Institute of Mental Health
Wade G. Regehr: Harvard Medical School
Mustafa Sahin: The F.M. Kirby Neurobiology Center, Boston Children’s Hospital, Harvard Medical School

Nature, 2012, vol. 488, issue 7413, 647-651

Abstract: Both heterozygous loss and homozygous loss of Tsc1 in mouse cerebellar Purkinje cells (PCs) result in autistic-like behaviours, which can be prevented by treatment with the mTOR inhibitor, rapamycin; these findings demonstrate critical roles for PCs in autistic-like behaviours in mice.

Date: 2012
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DOI: 10.1038/nature11310

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