RT Journal Article
SR Electronic
T1 The Sodium Channel <em>Scn8a</em> Is the Major Contributor to the Postnatal Developmental Increase of Sodium Current Density in Spinal Motoneurons
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 5234
OP 5239
DO 10.1523/JNEUROSCI.18-14-05234.1998
VO 18
IS 14
A1 Garcı́a, Kelly D.
A1 Sprunger, Leslie K.
A1 Meisler, Miriam H.
A1 Beam, Kurt G.
YR 1998
UL http://www.jneurosci.org/content/18/14/5234.abstract
AB 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.