Department of Neurology, Kobe University Graduate School of Medicine, Kobe City, Japan.
Clin Neurophysiol. 2012 Aug;123(8):1650-5. doi: 10.1016/j.clinph.2012.01.002. Epub 2012 Feb 14.
The molecular mechanisms underlying fibrillation potentials are still unclear. We hypothesised that expression of the cardiac-type voltage-gated sodium channel isoform Nav1.5 in denervated rat skeletal muscle is associated with the generation of such potentials.
Muscle samples were extracted and analysed biologically from surgically denervated rat extensor digitorum longus muscle after concentric needle electromyographic recording at various time points after denervation (4h to 6days).
Both nav1.5 messenger RNA (mRNA) signal on northern blotting and Nav1.5 protein expression on immunohistochemistry appeared on the second day after denervation, exactly when fibrillation potentials appeared. Administration of lidocaine, which has much stronger affinity for sodium channels in cardiac muscle than for those in skeletal muscle, dramatically decreased fibrillation potentials, but had no effect on contralateral compound muscle action potentials.
Expression of Nav1.5 participates in the generation of fibrillation potentials in denervated rat skeletal muscle.
We proposed an altered expression of voltage-gated sodium channel isoforms as a novel mechanism to explain the occurrence of fibrillation potentials following skeletal muscle denervation.
纤维颤搐电位产生的分子机制尚不清楚。我们假设，去神经支配大鼠骨骼肌中表达的心脏型电压门控钠离子通道亚型 Nav1.5 与这种电位的产生有关。
在去神经支配后（4 小时至 6 天）的各个时间点，通过同心针肌电图记录，从手术去神经支配的大鼠伸趾长肌中提取和分析肌肉样本。
在去神经后的第二天，Northern 印迹显示 nav1.5 信使 RNA（mRNA）信号，免疫组化显示 Nav1.5 蛋白表达，正好是纤维颤搐电位出现的时候。给予利多卡因，它对心肌钠通道的亲和力比骨骼肌钠通道强得多，可显著降低纤维颤搐电位，但对对侧复合肌肉动作电位无影响。
Nav1.5 的表达参与了去神经支配大鼠骨骼肌中纤维颤搐电位的产生。
我们提出了一种改变的电压门控钠离子通道亚型的表达，作为一种新的机制来解释去神经支配后纤维颤搐电位的发生。
