Lin Cindy S-Y, Kuwabara Satoshi, Cappelen-Smith Cecilia, Burke David
Prince of Wales Medical Research Institute, University of New South Wales, Australia.
J Physiol. 2002 Jun 15;541(Pt 3):1025-39. doi: 10.1113/jphysiol.2002.017848.
This study compared directly the post-ischaemic behaviour of sensory and motor axons in the human median nerve, focusing on the excitability changes produced by ischaemia and its release and by continuous polarizing DC. The decrease in threshold during ischaemia for 13 min was greater, the post-ischaemic increase in threshold was more rapid, and the return to the pre-ischaemic excitability took longer in sensory axons. However, a transient depolarizing threshold shift developed in sensory axons a few minutes after release of ischaemia. This pattern could not be reproduced by polarizing currents designed to mimic the probable pump-induced changes in membrane potential, even though the applied currents produced greater changes in threshold. Hyperpolarizing currents of equivalent intensity produced a greater increase in threshold for motor axons than sensory axons and, in studies of threshold electrotonus using graded hyperpolarizing DC, accommodation was greater in sensory than motor axons. The post-ischaemic changes in threshold were not uniform for axons of different threshold, whether sensory or motor, the threshold increase was usually less prominent for low-threshold axons. A transient post-ischaemic depolarization could be produced in motor axons with ischaemia of 20 min duration. Greater ischaemic and post-ischaemic changes in threshold for sensory axons could reflect greater dependence on the electrogenic Na+-K+ pump to maintain resting membrane potential and/or greater extracellular K+ accumulation in ischaemic sensory axons. Inward K+ currents due to extracellular K+ accumulation would then be more likely to trigger a depolarizing shift in membrane potential, the degree of K+ accumulation and pump activity being dependent on the duration of ischaemia. In sensory axons the greater tendency to accommodate to hyperpolarizing stimuli presumably contributes to shaping their post-ischaemic behaviour but is probably insufficient to explain why their behaviour differs from that of motor axons.
本研究直接比较了人类正中神经中感觉轴突和运动轴突缺血后的行为，重点关注缺血及其解除以及持续极化直流电所产生的兴奋性变化。感觉轴突在缺血13分钟期间阈值的降低幅度更大，缺血后阈值的升高更迅速，并且恢复到缺血前的兴奋性所需时间更长。然而，缺血解除后几分钟，感觉轴突会出现短暂的去极化阈值偏移。即使施加的电流在阈值上产生了更大的变化，但旨在模拟可能由泵引起的膜电位变化的极化电流并不能重现这种模式。等效强度的超极化电流对运动轴突阈值的升高幅度大于感觉轴突，并且在使用分级超极化直流电进行的阈下电紧张研究中，感觉轴突的适应性大于运动轴突。不同阈值的轴突（无论是感觉轴突还是运动轴突）缺血后的阈值变化并不一致，低阈值轴突的阈值升高通常不太明显。持续20分钟的缺血可在运动轴突中产生短暂的缺血后去极化。感觉轴突在缺血和缺血后阈值的变化更大，这可能反映出其对生电钠钾泵维持静息膜电位的依赖性更强和/或缺血性感觉轴突中细胞外钾离子积累更多。由于细胞外钾离子积累引起的内向钾电流更有可能触发膜电位的去极化偏移，钾离子积累程度和泵活性取决于缺血持续时间。在感觉轴突中，对超极化刺激的更大适应倾向可能有助于塑造其缺血后的行为，但可能不足以解释其行为与运动轴突不同的原因。
