The sodium channel Scn8a is the major contributor to the postnatal developmental increase of sodium current density in spinal motoneurons

Journal of Neuroscience

Volumn 18, Issue 14, 1998, Pages 5234-5239

  García, Kelly D ^a,c   Sprunger, Leslie K ^b   Meisler, Miriam H ^b   Beam, Kurt G ^a  

^a Department of Environmental and Radiological Health Sciences   (United States)

^b UNIVERSITY OF MICHIGAN MEDICAL SCHOOL   (United States)

^c UNIVERSITY OF ILLINOIS AT CHICAGO   (United States)

Author keywords

Motoneurons; Motor end plate disease; Mouse; Neuromuscular system; Postnatal development; Scn8a; Sodium channels

Indexed keywords

SODIUM CHANNEL;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CELL DENSITY; CONTROLLED STUDY; MOUSE; MUSCLE WEAKNESS; NERVE ENDING; NEUROMUSCULAR SYSTEM; NONHUMAN; PHENOTYPE; POSTNATAL DEVELOPMENT; PRIORITY JOURNAL; SODIUM CURRENT; SPINAL CORD MOTONEURON;

EID: 0032527590     PISSN: 02706474     EISSN: None     Source Type: Journal    
DOI: 10.1523/jneurosci.18-14-05234.1998     Document Type: Article

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