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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 Scn8asodium 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.

The Sodium ChannelScn8aIs the Major Contributor to the Postnatal Developmental Increase of Sodium Current Density in Spinal Motoneurons