Post-tetanic excitability changes and ectopic discharges in a human motor axon.

Post-tetanic ectopic discharges were studied in an identifiable human motor axon that could be stimulated non-invasively with high selectivity. This axon was tetanized at 300/s, for periods of 1-30 min, with 0.1 ms current pulses applied at the wrist. Repetitive discharges could be evoked by stimulation after tetani of 10 min or longer, and occurred spontaneously after tetani of 15 min or more. After a 20 min tetanus, bursts of up to 20 impulses at intervals of about 7 ms could be evoked for more than 30 min. Immediately after tetani of short duration, the threshold current required to excite the unit was increased, and it subsequently recovered monotonically. After tetani of 15 min or more, the threshold rose, then fell rapidly to below resting threshold, where it stayed for about as long as the stimuli evoked repetitive firing, before rising slowly to a second, broader maximum. The final recovery phase followed a stereotyped time course, whether starting immediately after a 3 min tetanus, or 2 h after a 30 min tetanus. When excitability was tested at defined intervals after the last impulse, abrupt transitions from low to high threshold were recorded, indicating that the axon could stay depolarized for at least 4 s after an impulse before rapidly hyperpolarizing. Repetitive discharges were evoked both when the threshold was low and when it was high, but the latency between the direct response and the start of the burst was different in the two cases. Only the short latency bursts, occurring at high threshold, were affected by polarizing currents applied at the stimulation site. The bursts at long latency (up to 200 ms) were presumed to originate elsewhere. Spontaneous bursts, occurring at intervals of 4-20 s, resembled the bursts which could be evoked by stimulation at about the same time. Our observations suggest that these post-tetanic ectopic discharges, like post-ischaemic motor discharges, occur on transitions from a hyperpolarized to a depolarized state. The transitions may occur spontaneously, but are readily triggered by an action potential, giving rise to a prolonged supernormal period. The bistability of the membrane potential probably occurs because accumulation of potassium ions under the myelin makes the currents through internodal potassium channels regenerative.