Bostock H, Grafe P
J Physiol. 1985 Aug;365:239-57. doi: 10.1113/jphysiol.1985.sp015769.
Myelinated nerve fibres with a reduced safety factor for conduction due to demyelination are easily blocked by trains of impulses. To find out why, in vivo recordings from rat ventral root fibres demyelinated with diphtheria toxin have been supplemented with in vivo and in vitro recordings from normal fibres. Despite a small rise in extracellular potassium activity, normal fibres were invariably hyperpolarized by intermittent trains of impulses. This hyperpolarization resulted in an increase in threshold and also in an enhancement of the depolarizing after-potential and the superexcitable period. Replacement of NaCl in the extracellular solution by LiCl completely blocked both the membrane hyperpolarization and the threshold increase which were normally observed during intermittent trains of impulses. At demyelinated nodes which were blocked by trains of impulses (10-50 Hz), conduction block was preceded by a rise in threshold current and in an increase in internodal conduction time, but by no detectable reduction in the outward current generated by the preceding node. It was found possible to prevent the threshold from changing during a train by automatic adjustment of a d.c. polarizing current. This 'threshold clamp' prevented the conduction failure and virtually abolished the changes in internodal conduction time. The threshold changes were attributed to hyperpolarization, as in normal fibres, since (a) the polarizing current required to prevent them was always a depolarizing current, and (b) they were accompanied by an increase in superexcitability. The post-tetanic depression that can follow continuous trains of impulses was attributed to the combination of increased threshold and enhanced superexcitable period due to hyperpolarization. It is concluded that the susceptibility of these demyelinated fibres to impulse trains is not due to a membrane depolarization induced by extracellular potassium accumulation but to a membrane hyperpolarization as a consequence of electrogenic sodium pumping.
由于脱髓鞘导致传导安全系数降低的有髓神经纤维很容易被一连串冲动所阻断。为了找出原因，对白喉毒素诱导脱髓鞘的大鼠腹根纤维进行的体内记录，补充了来自正常纤维的体内和体外记录。尽管细胞外钾活性略有升高，但正常纤维总是被间歇性冲动串超极化。这种超极化导致阈值升高，同时也增强了去极化后电位和超兴奋性时期。用氯化锂替代细胞外溶液中的氯化钠，完全阻断了在间歇性冲动串期间通常观察到的膜超极化和阈值升高。在被冲动串（10 - 50Hz）阻断的脱髓鞘节段，传导阻滞之前阈值电流升高，节间传导时间增加，但前一个节段产生的外向电流没有可检测到的减少。发现通过自动调节直流极化电流可以防止冲动串期间阈值发生变化。这种“阈值钳制”防止了传导失败，并几乎消除了节间传导时间的变化。阈值变化归因于超极化，就像在正常纤维中一样，因为（a）防止阈值变化所需的极化电流总是去极化电流，并且（b）它们伴随着超兴奋性的增加。连续冲动串后可能出现的强直后抑制归因于由于超极化导致的阈值升高和超兴奋性时期增强的综合作用。得出的结论是，这些脱髓鞘纤维对冲动串敏感不是由于细胞外钾积累引起的膜去极化，而是由于电生性钠泵导致的膜超极化。
