Organized cultures of mammalian spinal and dorsal root ganglions were used for a comparative study of the neurocytopathology caused by rabies and so-called rabies-like viruses. Electron microscopy and titration of infectivity revised earlier data in which no difference could be demonstrated between street and fixed-virus infection. In the present study, fixed virus produced inclusion bodies without apparent virus assembly. Sequential electron microscopy revealed that the main sites of virus assembly were the membranes of the Golgi complex. In contrast, rabies-like viruses freshly isolated from wild rodents produced inclusion bodies all of which were associated with virus replication. Electron microscopic evidence has led us to classify these strains as street virus. Nonneural cell elements from cultivated ganglions were susceptible to fixed virus and the cultures yielded higher titers of infectivity as compared to those of rabies-like viruses. Virus budding was shown to occur at the cell surface as well as at intracytoplasmic membranes.