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The Journal of Neuroscience, July 15, 1998, 18(14):5234-5239

The Sodium Channel Scn8a Is the Major Contributor to the Postnatal Developmental Increase of Sodium Current Density in Spinal Motoneurons

Kelly D. García¹, Leslie K. Sprunger², Miriam H. Meisler², and Kurt G. Beam¹

¹ Department of Anatomy and Neurobiology, Colorado State University, Fort Collins, Colorado 80523-1670, and ² Department of Human Genetics, University of Michigan, Ann Arbor, Michigan 48109-0618

Sodium currents were recorded from motoneurons that were isolated from mice at postnatal days 0-8 (P0-P8) and maintained in culture for 12-24 hr. Motoneurons from normal mice exhibited a more than threefold increase in peak sodium current density from P0 to P8. For mice lacking a functional Scn8a sodium channel gene, motoneuronal sodium current density was comparable at P0 to that of normal mice but failed to increase from P0 to P8. The absence of Scn8a sodium channels is associated with the phenotype "motor end plate disease," which is characterized by a progressive neuromuscular failure and is fatal by 3-4 postnatal weeks. Thus, it appears that the development and function of mature motoneurons depends on the postnatal induction of Scn8a expression.

Key words: motoneurons; sodium channels; Scn8a; postnatal development; motor end plate disease; neuromuscular system; mouse

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Copyright © 1998 Society for Neuroscience  0270-6474/98/18145234-06$05.00/0

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