Responses of human sensory and motor axons to the release of ischaemia and to hyperpolarizing currents.
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.
Lin
Cindy S-Y
CS
Prince of Wales Medical Research Institute, University of New South Wales, Australia.
Kuwabara
Satoshi
S
Cappelen-Smith
Cecilia
C
Burke
David
D
D000293:Adolescent; D000328:Adult; D001369:Axons / Q000502:physiology*; D004558:Electric Stimulation; D004594:Electrophysiology; D005260:Female; D006801:Humans; D007473:Ion Channels / Q000502:physiology; D007511:Ischemia / Q000503:physiopathology; D008297:Male; D008475:Median Nerve / Q000098:blood supply / Q000503:physiopathology*; D008875:Middle Aged; D009046:Motor Neurons / Q000502:physiology*; D009475:Neurons, Afferent / Q000502:physiology*; D011188:Potassium / Q000378:metabolism; D015221:Potassium Channels / Q000378:metabolism; D012039:Regional Blood Flow / Q000502:physiology; D000254:Sodium-Potassium-Exchanging ATPase / Q000502:physiology
D007473:Ion Channels; D015221:Potassium Channels; D000254:Sodium-Potassium-Exchanging ATPase; D011188:Potassium