Moldovan Mihai, Krarup Christian
Division of Neurophysiology, Institute of Medical Physiology, Panum Institute and the Department of Clinical Neurophysiology, the Neuroscience Center, Rigshospitalet, University of Copenhagen, 2100 Copenhagen, Denmark.
J Physiol. 2004 Nov 1;560(Pt 3):807-19. doi: 10.1113/jphysiol.2004.069443. Epub 2004 Aug 5.
We found persistent abnormalities in the recovery of membrane excitability in long-term regenerated motor nerve fibres in the cat as indicated in the companion paper. These abnormalities could partly be explained by membrane hyperpolarization. To further investigate this possibility, we compared the changes in excitability in control nerves and long-term regenerated cat nerves (3-5 years after tibial nerve crush) during manoeuvres known to alter axonal membrane Na(+)-K(+) pump function: polarization, cooling to 20 degrees C, reperfusion after 10 min ischaemia, and up to 60 s of repetitive stimulation at 200 Hz. The abnormalities in excitability of regenerated nerves were reduced by depolarization and cooling and increased by hyperpolarization and during postischaemia. Moreover, the time course of recovery of excitability from repetitive stimulation and ischaemia was prolonged in regenerated nerves. Our data are consistent with an increased demand for electrogenic Na(+)-K(+) pumping in regenerated nerves leading to membrane hyperpolarization. Such persistent hyperpolarization may influence the ability of the axon to compensate for changes in membrane potential following normal repetitive activity.
正如配套论文中所指出的,我们发现猫的长期再生运动神经纤维在膜兴奋性恢复方面存在持续异常。这些异常部分可由膜超极化来解释。为了进一步探究这种可能性,我们比较了对照神经和猫的长期再生神经(胫神经挤压后3 - 5年)在已知会改变轴突膜钠钾泵功能的操作过程中的兴奋性变化:极化、冷却至20摄氏度、缺血10分钟后的再灌注以及以200赫兹进行长达60秒的重复刺激。再生神经兴奋性的异常在去极化和冷却时降低,在超极化时以及缺血后增加。此外,再生神经从重复刺激和缺血中恢复兴奋性的时间进程延长。我们的数据与再生神经中对电生性钠钾泵浦的需求增加导致膜超极化一致。这种持续的超极化可能会影响轴突在正常重复活动后补偿膜电位变化的能力。