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1. In crayfish, the normally passive, non-spiking somata of certain unipolar, efferent neurones became spiking within 36 hr of axotomy. 2. The changes persisted for approximately 2 weeks and then waned. The decline in excitability occurred independently of regeneration, and excitability was not restored by recutting the axon stump. 3. The neuropilar processes also became capable of supporting spikes, but synaptic transmission onto the cells and the spike threshold for orthodromic activation were unchanged, as was the gross structure of the neurone. 4. In somata which normally spike, electrogenicity was nevertheless increased, as evidenced by soma spikes that were larger, faster rising, and easier to evoke. 5. We tested for post-axotomy excitability changes in a variety of identified neurones. Every type (n = 5) of phasically active efferent we tested responded as above, as did all three phasic interneurones. One class of spontaneously active interneurones and one spontaneously active efferent did not respond to axotomy. 6. Extensive damage to afferents did not initiate changes in efferents of the same ganglion, nor did it interfere with changes induced by axotomy of the efferents. 7. Transection of the larger of the two main branches of the phasic flexor inhibitor induced soma excitability, but cutting the smaller branch did not. However, after the excitability caused by cutting the larger branch waned, transection of the smaller branch then induced excitability. 8. Neurones with longer axon stumps took longer to develop soma excitability.

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