Diseases of the central nervous system with limited prognosis, as multiple sclerosis, have led to the development of experimental models to study the pathophysiology of such diseases. The present investigation deals with the ethidium bromide (EB) model of demyelination with the objective to study the pathogenesis of encephalic demyelinating lesions. A single 10 microliters injection of 0.1% EB in 0.15 M saline was inoculated in the ventral surface of the pons of adult Wistar rats and after times ranging from 24 h to 30 days, the animals were anaesthetized and perfused with Karnovsky fixative for light and electron microscopy studies. From 3 to 7 days after the EB injection the tissue had developed a spongiotic aspect with intra- and extracellular swelling, demyelinating fibers and a number of necrotic glial cells. By 11 days the reactive phase had begun, and a large number of macrophages had migrated to the foci of the lesion, initiating the absorption of the necrotic tissue. In addition, there were oligodendrocyte-remyelinating nerve fibers and astrocytic gliosis. At 15 days Schwann cells-remyelinating fibers were first seen at the periphery of the lesion while the central area acquired a cystic pattern. The results obtained with the EB-demyelinating model in brain of adult rats showed that 1) remyelination by oligodendrocytes surpassed that by Schwann cells and 2) astrocytic processes were present at the areas remyelinated by the former and absent from those remyelinated by the latter.30341-8