Figure 1. Depiction of the preparation and description of measured parameters.

A, the preparation, showing recording via an intracellular electrode (which in some experiments was also used for stimulation), axonal stimulation and the peripheral axonal injury at the level of the spinal nerve. Components are not to scale. B, measurements determined from action potential (AP) trace. AHP80%, duration of afterhyperpolarization until 80% recovery to baseline; AHPamp, amplitude of afterhyperpolarization; AHParea, area of the afterhyperpolarization; AHPd, afterhyperpolarization duration; APamp, amplitude of AP; APd, duration of the AP at 95% repolarization; RMP, resting membrane potential. C, AP trace (above) and differentiated wave (below) from an A_o-type neuron that lacks an inflection on the descending limb of the AP. D, AP trace (above) and differentiated wave (below) from an A_i-type neuron, showing an inflection on the descending limb of the AP, as confirmed in the differentiated trace with an interval of decreased negative slope (arrows). Note C and D have different V s⁻¹ and time scales. E and F, somatic voltage traces during paired axonal stimulation in two different neurons. Recordings of successively shorter interstimulus intervals are superimposed. Stimuli are evident as downward deflections in the voltage traces. The neuron in E shows failure of conduction into the soma at a RP of 1.3 ms, at which interval there is a complete absence of a somatic voltage response. The neuron in F shows failure of full somatic invasion at a RP of 1.4 ms, at which interval there is a decreased somatic depolarization (single arrow), representing a passive electrotonic potential. The final complete failure of propagation of the second AP (double arrow) occurs at a shorter interstimulus interval. The electrotonic potentials (single arrow) represent AP failure in the stem axon, while complete absence of an impulse (double arrow) represents failure at the T-junction.