Motor disturbances in mice with deficiency of the sodium channel gene Scn8a show features of human dystonia
- 31 December 2003
- journal article
- Published by Elsevier in Experimental Neurology
- Vol. 184 (2) , 830-838
- https://doi.org/10.1016/s0014-4886(03)00290-5
Abstract
No abstract availableKeywords
This publication has 35 references indexed in Scilit:
- Voltage‐gated Sodium Channels in EpilepsyEpilepsia, 2002
- Molecular and pathological effects of a modifier gene on deficiency of the sodium channel Scn8a (Nav1.6)Human Molecular Genetics, 2002
- Dopamine transmission in DYT1 dystonia: A biochemical and autoradiographical studyNeurology, 2002
- Sodium channel Na v 1.6 is localized at nodes of Ranvier, dendrites, and synapsesProceedings of the National Academy of Sciences, 2000
- Differences in anxiety-related behaviours and in sensitivity to diazepam in inbred and outbred strains of micePsychopharmacology, 2000
- Paroxysmal kinesigenic choreoathetosis: a report of 26 patientsZeitschrift für Neurologie, 1999
- The Sodium ChannelScn8aIs the Major Contributor to the Postnatal Developmental Increase of Sodium Current Density in Spinal MotoneuronsJournal of Neuroscience, 1998
- Mutation Detection in the and Alleles of the Sodium ChannelJournal of Biological Chemistry, 1996
- Paroxysmal dyskinesias: Clinical features and classificationAnnals of Neurology, 1995
- Hereditary motor end-plate disease in the mouse: light and electron microscopic studies.Journal of Neurology, Neurosurgery & Psychiatry, 1970