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Experiments showed co-contraction of opposing muscle groups, and indicated that symptoms depended on the interaction of brain and spinal cord. SNP mapping and exome sequencing identified the dominant causative mutation in the Lamb1 gene. Laminins are extracellular matrix proteins, widely expressed but also known to be important in synapse structure and plasticity. In accordance, awake recording in the cerebellum detected abnormal output from a circuit of two Lamb1-expressing neurons, Purkinje cells and their deep cerebellar nucleus targets, during abnormal postures. We propose that dystonia-like symptoms result from lapses in descending inhibition, exposing excess activity in intrinsic spinal circuits that coordinate muscles. The mouse is a new model for testing how dysfunction in the CNS causes specific abnormal movements and postures.<\/jats:p>","DOI":"10.7554\/elife.11102","type":"journal-article","created":{"date-parts":[[2015,12,24]],"date-time":"2015-12-24T07:38:55Z","timestamp":1450942735000},"source":"Crossref","is-referenced-by-count":33,"title":["A dystonia-like movement disorder with brain and spinal neuronal defects is caused by mutation of the mouse laminin \u03b21 subunit, Lamb1"],"prefix":"10.7554","volume":"4","author":[{"given":"Yi Bessie","family":"Liu","sequence":"first","affiliation":[{"name":"Department of Neurosurgery, Massachusetts General Hospital, Harvard Medical School, Boston, United States"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ambika","family":"Tewari","sequence":"additional","affiliation":[{"name":"Dominick P. 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