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This Article Full Text Full Text (PDF) All Versions of this Article: 564/3/931    most recent jphysiol.2005.083394v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Bostock, H. Articles by Burke, D. Search for Related Content PubMed PubMed Citation Articles by Bostock, H. Articles by Burke, D.

¹ Sobell Department of Neurophysiology, Institute of Neurology, Queen Square, London, UK and Institute of Clinical Neurosciences
² The University of Sydney and Royal Prince Alfred Hospital, Sydney, Australia

Subthreshold electrical stimuli can generate a long-lasting increase in axonal excitability, superficially resembling the phase of superexcitability that follows a conditioning nerve impulse. This phenomenon of ‘subthreshold superexcitability’ has been investigated in single motor axons in six healthy human subjects, by tracking the excitability changes produced by conditioning stimuli of different amplitudes and waveforms. Near-threshold 1 ms stimuli caused a mean decrease in threshold at 5 ms of 22.1 ± 6.0% (mean ±S.D.) if excitation occurred, or 6.9 ± 2.6% if excitation did not occur. The subthreshold superexcitability was maximal at an interval of about 5 ms, and fell to zero at 30 ms. It appeared to be made up of two components: a passive component linearly related to conditioning stimulus amplitude, and a non-linear active component. The active component appeared when conditioning stimuli exceeded 60% of threshold, and accounted for a maximal threshold decrease of 2.6 ± 1.3%. The passive component was directly proportional to stimulus charge, when conditioning stimulus duration was varied between 0.2 and 2 ms, and could be eliminated by using triphasic stimuli with zero net charge. This change in stimulus waveform had little effect on the active component of subthreshold superexcitability or on the ‘suprathreshold superexcitability’ that followed excitation. It is concluded that subthreshold superexcitability in human motor axons is mainly due to the passive electrotonic effects of the stimulating current, but this is supplemented by an active component (about 12% of suprathreshold superexcitability), due to a local response of voltage-dependent sodium channels.

(Received 20 January 2005; accepted after revision 28 February 2005; first published online 3 March 2005)
Corresponding author H. Bostock: Sobell Department, Institute of Neurology, Queen Square, London WC1N 3BG, UK. Email: h.bostock{at}ion.ucl.ac.uk