The cell body of the medial giant interneuron (MGI) in the cricket normally does not spike in response to injected depolarizing currents. When axotomized 1 mm or more from the cell body (distant axotomy), the membrane properties of the soma remain unchanged. However, after axotomy close to the cell body (200 to 500 micron), the soma membrane becomes capable of generating action potentials by 6 hr after lesion. These regenerative spikes are 1 to 1.5 msec in duration and may reach 100 mV in peak amplitude. Ion substitutions indicate that these action potentials are primarily sodium dependent. A calcium-dependent component of soma membrane excitability that is normally present appears to be unaffected by axotomy. By 48 hr, the close axotomized MGI somata have lost the ability to generate action potentials and the membrane electrical properties return to normal. By 2 days after axotomy close to the soma, large, membrane-bound, electron-lucent vacuoles appear in the cytoplasm of the MGI cell body. Such vacuoles then disappear from axotomized MGI somata by 10 days. In addition, numerous arrays of densely packed, darkly staining microtubules are observed in the cell body, especially concentrated near the initial neurite. Neither of these specialized structures is observed in control, intact MGI somata. We propose that close axotomy disrupts the mechanisms which regulate the stability of the fully mature, differentiated neuron. The characteristic morphological and physiological stability of the MGI is lost: the dendritic arborization has been shown previously to be altered by extensive new outgrowth (Roederer, E., and M. J. Cohen (1983) J. Neurosci. 3: 1835-1847); there is a transient increase in soma membrane excitability, and new cytoplasmic organelles are induced.