INVESTIGADORES
DORFMAN Damian
artículos
Título:
Ischemic conditioning protects from axoglial alterations of the optic pathway induced by experimental diabetes in rats
Autor/es:
FERNANDEZ DC; PASQUINI LA; DORFMAN D; ALDANA MARCOS HJ; ROSENSTEIN RE
Revista:
PLOS ONE
Editorial:
PUBLIC LIBRARY SCIENCE
Referencias:
Lugar: San Francisco; Año: 2012 vol. 7 p. 51966 - 51976
ISSN:
1932-6203
Resumen:
PLoS One. 2012;7(12):e51966. doi: 10.1371/journal.pone.0051966. Epub 2012 Dec 20.
Ischemic conditioning protects from axoglial alterations of the optic pathway induced by experimental diabetes in rats.
Fernandez DC, Pasquini LA, Dorfman D, Aldana Marcos HJ, Rosenstein RE.
Source
Laboratory
of Retinal Neurochemistry and Experimental Ophthalmology, Department of
Human Biochemistry, School of Medicine, University of Buenos
Aires/CEFyBO, CONICET, Buenos Aires, Argentina.
Abstract
Diabetic
retinopathy is a leading cause of blindness. Visual function disorders
have been demonstrated in diabetics even before the onset of
retinopathy. At early stages of experimental diabetes, axoglial
alterations occur at the distal portion of the optic nerve. Although
ischemic conditioning can protect neurons and synaptic terminals against
ischemic damage, there is no information on its ability to protect
axons. We analyzed the effect of ischemic conditioning on the early
axoglial alterations in the distal portion of the optic nerve induced by
experimental diabetes. Diabetes was induced in Wistar rats by an
intraperitoneal injection of streptozotocin. Retinal ischemia was
induced by increasing intraocular pressure to 120 mm Hg for 5 min; this
maneuver started 3 days after streptozotocin injection and was weekly
repeated in one eye, while the contralateral eye was submitted to a sham
procedure. The application of ischemia pulses prevented a deficit in
the anterograde transport from the retina to the superior colliculus, as
well as an increase in astrocyte reactivity, ultraestructural myelin
alterations, and altered morphology of oligodendrocyte lineage in the
optic nerve distal portion at early stages of experimental diabetes.
Ischemia tolerance prevented a significant decrease of retinal glutamine
synthetase activity induced by diabetes. These results suggest that
early vision loss in diabetes could be abated by ischemic conditioning
which preserved axonal function and structure.