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Distribution of GAP-43 was studied in the retinas of rats after continuous illumination followed by different darkness periods. GAP-43 immunoreactivity was maximum in regenerating outer photoreceptor segments of rats kept in total darkness for 10 days, while in the inner plexiform layer, immunoreactivity was maximum immediately after illumination. Changes in GAP-43 expression could participate in retinal repair/regeneration after light-induced damage.

Shiga toxin (Stx) from enterohemorrhagic Escherichia coli (STEC) is the main cause of hemorrhagic colitis which may derive into Hemolytic Uremic Syndrome (HUS) and acute encephalopathy, one of the major risk factors for infant death caused by the toxin. We have previously demonstrated that intracerebroventricular administration of Stx2 causes neuronal death and glial cell damage in rat brains. In the present work, we observed that the intracerebroventricular administration of Stx2 increased the expression of glial fibrillary acidic protein (GFAP) leading to astrogliosis. Confocal microscopy showed reactive astrocytes in contact with Stx2-containing neurons. Immunocolocalization of increased GFAP and Stx2 in astrocytes was also observed. This insult in the brain was correlated with changes in the expression and activity of neuronal nitric oxide synthase (nNOS) by using the NADPH-diaphorase histochemical technique (NADPH-d HT). A significant decrease in NOS/NADPH-d-positive neurons and NOS/NADPH-d activity was observed in cerebral cortex and striatum, whereas an opposite effect was found in the hypothalamic paraventricular nucleus. We concluded that the i.c.v. administration of Stx2 promotes a typical pattern of brain injury showing reactive astrocytes and an alteration in the number and activity of nNOS/NADPH-d. According to the functional state of nNOS/NADPH-d and to brain cell morphology data, it could be inferred that the i.c.v. administration of Stx2 leads to either a neurodegenerative or a neuroprotective mechanism in the affected brain areas. The present animal model resembles the encephalopathy developed in Hemolytic Uremic Syndrome (HUS) patients by STEC intoxication. Fil: Boccoli, Javier. Universidad de Buenos Aires. Facultad de Medicina; Argentina Fil: Loidl, Cesar Fabian. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Biología Celular y Neurociencia "Prof. Eduardo de Robertis". Universidad de Buenos Aires. Facultad de Medicina. Instituto de Biología Celular y Neurociencia; Argentina Fil: López, Juan José. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Biología Celular y Neurociencia "Prof. Eduardo de Robertis". Universidad de Buenos Aires. Facultad de Medicina. Instituto de Biología Celular y Neurociencia; Argentina Fil: Pistone Creydt, Virginia. Universidad de Buenos Aires. Facultad de Medicina; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Ibarra, Cristina Adriana. Universidad de Buenos Aires. Facultad de Medicina; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Goldstein Raij, Jorge. Universidad de Buenos Aires. Facultad de Medicina; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina

Illumination produces degeneration of outer photoreceptor segments, a phenomenon that may be reversed after a period of darkness. Neuronal expression of the immediate early genes (IEGs) c-fos and c-jun, both recognized as proto-oncogenes, has been reported after stimulation of different regions in the central nervous system (CNS). We performed a sequential study on Fos and Jun immunoreactivity to investigate the role of IEGs following 8 days of continuous illumination in 30–35-day-old Wistar rats. Retinas were fixed by perfusion in 4% paraformaldehyde, after a period of illumination followed by 0, 2, 7, 10 and 20 days in total darkness. Cryostat sections were immunocytochemically stained using antibodies to Fos and Jun. Fos and Jun immunoreactivities were detected in all photoreceptors evaluated, peaking in nuclei of rats kept in total darkness for 2 days, and becoming negative as from 7 days. Increases in c-fos and c-jun products during the darkness period may play a role in triggering molecular events participating in plastic changes in photoreceptors and/or in the protection from oxidative damage caused by free radicals induced by light irradiation.