After cervical dorsal rhizotomy, small dark central terminals (C1) of glomeruli underwent electron dense changes at 8 h and were all degenerated at 36 h; their number persisted, though slightly diminished, up to 15 days, glial engulfment being negligible. Light large central terminals without neurofilaments (CIIa) showed electron-lucent or electron-dense degeneration from 14 to 36 h, while those with neurofilaments (CIIb) exhibited increased neurofilamentous areas, with depletion and presynaptic concentration of synaptic vesicles as in the electron-lucent change, at the 8-36 h postrhizotomy periods. Both CII-varieties were all degenerated at 36 h and became electron dense at 48 h; glial phagocytosis was intense and no terminals were present after 4 days. It is concluded that in the rat the 3 types of central glomerular terminals are primary axons, and that each type undergoes a different pattern of degeneration which points to a separate primary afferent origin. Numerous nonglomerular axodendritic endings began showing electron-dense degeneration at 8 h which rapidly masked their normal structure, although most appeared to contain round agranular vesicles, and some of them dense-cored vesicles (in lamina I). A few endings exhibited electron-lucent degeneration. Labeling methods seem preferable for studying the primary origin of nonglomerular terminals, due to the difficulty in recognizing the normal predegenerative structure of these profiles.