We have previously studied accommodation in rat and human motor axons by testing excitability with combinations of long and short current pulses. We found that normally polarized axons accommodate slowly and partially (over about 50 ms) to subthreshold depolarizing currents, and that the principal mechanism is the activation of slow potassium channels (Bostock & Baker, 1988). To understand the response of human nerves to ischaemia, we have now extended these observations to axons already depolarized before the testing currents were applied. 2. Rat ventral root axons were depolarized by passing continuous currents or by raising the extracellular potassium concentration. Human forearm nerves were depolarized by ischaemia, induced by inflating a sphygmomanometer cuff on the upper arm. Depolarized rat and human motor axons accommodated much more rapidly and completely than normally polarized axons (e.g. accommodation in rat axons was 50% complete within 2 ms at about 15 mV depolarized to rest). 3. The fast component of accommodation in depolarized rat fibres was not blocked by tetraethylammonium ions or 4-aminopyridine, was not accompanied by a conductance or potential change, and had a time constant of 1.7 ms at 30 degrees C. It was attributed to inactivation of closed sodium channels. 4. In depolarized rat fibres exhibiting fast accommodation, a brief rise in excitability was seen at the break of an anodal current. Our prediction that human motor axons would show anode-break excitation during ischaemia was readily confirmed. 5. The results are discussed in relation to Hill's (1936) mathematical description of accommodation in nerve, and it is concluded that his description is only applicable to depolarized axons.
