Proliferating cells in the subventricular zone (SVZ) of adult rat brain could provide a source of cells for repair attempts during degenerative diseases. However, very few reports dealt with the spontaneous regulation of this cell population during experimental conditions. In this paper, we describe an increase in the proliferation activity in the SVZ during experimental allergic encephalomyelitis, a demyelinating disease widely used as an experimental model for human multiple sclerosis. Moreover, p75 LNGFR -immunoreactive elements in the SVZ were larger in experimental allergic encephalomyelitis compared with control groups, and they also showed multiple and branched elongations. Finally, a selective uptake of 125 I-nerve growth factor was observed in the SVZ in neonatal rats, and positive elements migrated in the corpus callosum within a few days. These data indicate that cell populations in the SVZ are regulated during inf lammatory conditions and degenerative diseases involving oligodendrocytes and neurotrophins, including nerve growth factor, could participate in these phenomena.The repair capability of the nervous system is extremely low in adult life, in view of the postmitotic nature of neural and glial elements. This at least partially accounts for the devastating consequences of acute damage (i.e., stroke, trauma, etc.) and long-lasting neurodegenerative processes (i.e., Alzheimer's disease, Parkinson's disease, multiple sclerosis, etc.). Experimental allergic encephalomyelitis (EAE) and multiple sclerosis are degenerative diseases characterized by the severe loss of oligodendrocytes and consequent demyelination, probably caused by inflammatory and autoimmune components. We previously have reported that nerve growth factor (NGF) increases in the cerebrospinal fluid of patients affected by multiple sclerosis (1) and also in brain areas of rats during EAE (2), where p75 LNGFR immunoreactivity also is strongly upregulated according to the severity of inflammatory cellular infiltrate (2). These and other data suggest a functional relation between the NGF level, p75 LNGFR regulation, and the stage of the disease. In these conditions, NGF and related neurotrophins, such as other growth factors, are believed to play a major role in protection such as repair attempts. However, effective strategies to transfer successful experimental approaches aiming at manipulating endogenous levels of neurotrophins to stimulate protective and repair phenomena in humans are not still available.The recent discovery of multipotent dividing, epidermal growth factor-sensitive cells in the subventricular zone (SVZ) of the mature central nervous system (CNS) in rodents and also in humans has offered a new potentiality for brain repair strategies. This large population of rapidly and constitutively proliferating cells gives rise not only to periglomerular neurons and interneurons in the olfactory bulb, but also to glial cells including oligodendrocytes (3, 4). In vivo (5) and in vitro (6) studies have indicated that growth f...
