Willow M, Taylor S M, Catterall W A, Finnell R H
Cell Mol Neurobiol. 1986 Jun;6(2):213-20. doi: 10.1007/BF00711071.
Tottering mice, in which a single gene lesion leads to prolonged hyperexcitability and spontaneous epilepsy, were studied to determine whether enhanced electrical activity leads to down regulation of sodium channels in central neurons. The number of sodium channels in synaptosomes, as assessed by saxitoxin binding, was decreased from 5.38 +/- 0.06 pmol/mg protein in coisogenic controls to 3.85 +/- 0.10 pmol/mg protein (P less than 0.001) in tottering mice without a change in the KD for saxitoxin. Neurotoxin-activated 22Na+ influx per sodium channel was increased 80% in tottering mice (P less than 0.001). Evidently, the increased level of electrical excitability characteristic of the tottering phenotype causes down regulation of the sodium-channel number and alteration of channel function in the nerve terminals of central neurons.
蹒跚小鼠由于单个基因损伤导致长时间的过度兴奋和自发性癫痫，对其进行研究以确定增强的电活动是否会导致中枢神经元中钠通道的下调。通过石房蛤毒素结合评估，突触体中钠通道的数量从同基因对照中的5.38±0.06 pmol/mg蛋白质减少到蹒跚小鼠中的3.85±0.10 pmol/mg蛋白质（P<0.001），而石房蛤毒素的解离常数（KD）没有变化。在蹒跚小鼠中，每个钠通道的神经毒素激活的22Na+内流增加了80%（P<0.001）。显然，蹒跚表型所特有的电兴奋性增加水平导致中枢神经元神经末梢中钠通道数量的下调和通道功能的改变。
