The gliotoxic chemical ethidium bromide when injected locally in the rat spinal cord induced areas of demyelination which developed at various times according to the dose used. High doses induced lesions of fast development (type I) and intermediate lesions (type III) whereas low doses induced slow lesions (type II). Following the demyeli-nating process, naked axons were remyelinated either by oligodendrocytes or Schwann cells (SC) depending on their location in areas respectively with or without astrocytes. In most lesions the area remyelinated by SC was proeminent. In lesions of slow development it was possible to observe the factors that influenced SC behavior within the central nervous system. Following the initial invasion from subpial areas and perivascular spaces, SC expansion depended on the presence of a stable extracellular matrix. In type I lesions this matrix was present due to the inflammatory nature of the process. In tipe II lesions that matrix did not occur thus SC only could migrate among demyelinated axons using them as stepping stones. Between adjacent SC thin diameter collagen fibres could be detected. It was not found any evidence of SC migration along the naked axons.