Axonopatía distal temprana de la vía visual en la diabetes experimental: Efecto terapéutico de la inducción de tolerancia isquémica

DIEGO C. FERNANDEZ, LAURA A. PASQUINI, DAMIÁN DORFMAN, HERNÁN J. ALDANA MARCOS, RUTH E. ROSENSTEIN

Mar del Plata

Congreso; LVI Reunión Científica Anual Sociedad Argentina de Investigación Clínica (SAIC); 2011

SAIC

Diabetic retinopathy is a leading cause of acquired blindness. Visual function disorders have been demonstrated in diabetics with very early retinopathy or even before the onset of retinopathy. The aim of the present work was to analyze the visual pathway in an early step of experimental diabetes. Diabetes was induced in Wistar rats by an intraperitoneal injection of streptozotocin. A deficit in the anterograde transport from the retina to the superior colliculus at 6 weeks post-injection of streptozotocin was observed. At this time point, morphological studies did not reveal retinal ganglion cell loss or substantial alterations in the superior colliculus. The optic nerve was morphometrically evaluated at intraorbital (unmyelinated and myelinated) and intracranial sections. In animals that had been diabetic for 6 weeks, a large increase in astrocyte reactivity occurred in the distal (but not intraorbital) portion, which coincided with a significant axon loss. Moreover, profound myelin alterations and altered morphology of oligodendrocyte lineage were observed at the distal optic nerve (but not proximal) portion. The present results suggest that axoglial alterations at the distal portion of the optic nerve could be the first structural change in the diabetic visual pathway. Wistar rats by an intraperitoneal injection of streptozotocin. A deficit in the anterograde transport from the retina to the superior colliculus at 6 weeks post-injection of streptozotocin was observed. At this time point, morphological studies did not reveal retinal ganglion cell loss or substantial alterations in the superior colliculus. The optic nerve was morphometrically evaluated at intraorbital (unmyelinated and myelinated) and intracranial sections. In animals that had been diabetic for 6 weeks, a large increase in astrocyte reactivity occurred in the distal (but not intraorbital) portion, which coincided with a significant axon loss. Moreover, profound myelin alterations and altered morphology of oligodendrocyte lineage were observed at the distal optic nerve (but not proximal) portion. The present results suggest that axoglial alterations at the distal portion of the optic nerve could be the first structural change in the diabetic visual pathway.