Axotomy induces a transient change in the soma membrane from non-spiking to spiking in many neurones of the crayfish abdominal C.N.S. The ionic and metabolic dependence of this phenomenon was investigated in one identified neurone. 2. The inward current of axotomy-induced soma spikes is carried primarily by Na ions. 3. Addition of 50 mM-tetraethylammonium to the external saline unmasks predominantly Ca-mediated soma spikes in control cells. The calcium spikes are not affected by axotomy. 4. Axotomy induces a transient increase in delayed rectification of the soma membrane. 5. Membrane potential is dependent on the external potassium concentration as predicted by the Nernst function while external sodium has essentially no effect. This is not changed following axotomy. 6. The inward current of the axon spike is primarily carried by sodium ions both before and after axotomy. The overshoot of the axon spike is not dramatically changed between the time when axotomy-induced soma spikes are present and when they have disappeared. 7. Following axotomy, both the onset and offset of axotomy-induced soma spikes occur earlier when the temperature is raised by 10 degrees C. 8. Cycloheximide retards or prevents soma spikes normally seen following axotomy. 9. The results indicate that axotomy induces a transient increase in voltage-dependent Na and K conductances but not Ca conductance, and that these changes are dependent on axotomy-inhibited protein synthesis.
