钠通道Scn8a是脊髓运动神经元钠电流密度出生后发育性增加的主要促成因素。
The sodium channel Scn8a is the major contributor to the postnatal developmental increase of sodium current density in spinal motoneurons.
作者信息
García K D, Sprunger L K, Meisler M H, Beam K G
机构信息
Department of Anatomy and Neurobiology, Colorado State University, Fort Collins, Colorado 80523-1670, USA.
出版信息
J Neurosci. 1998 Jul 15;18(14):5234-9. doi: 10.1523/JNEUROSCI.18-14-05234.1998.
Abstract
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.
摘要
从出生后0 - 8天（P0 - P8）的小鼠中分离出运动神经元，并在培养中维持12 - 24小时后记录钠电流。正常小鼠的运动神经元从P0到P8的峰值钠电流密度增加了三倍多。对于缺乏功能性Scn8a钠通道基因的小鼠，运动神经元钠电流密度在P0时与正常小鼠相当，但从P0到P8未能增加。Scn8a钠通道的缺失与“运动终板疾病”表型相关，其特征是进行性神经肌肉衰竭，在出生后3 - 4周内致命。因此，成熟运动神经元的发育和功能似乎依赖于出生后Scn8a表达的诱导。
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