May 2003
Volume 44, Issue 13
ARVO Annual Meeting Abstract  |   May 2003
Vascular and Glial Changes in Early Stages of Light-Induced Retinal Degeneration
Author Affiliations & Notes
  • A.M. Suburo
    Facultad de Ciencias Biomédicas, Universidad Austral, Buenos Aires, Argentina
  • V. Torbidoni
    Facultad de Ciencias Biomédicas, Universidad Austral, Buenos Aires, Argentina
  • Footnotes
    Commercial Relationships  A.M. Suburo, None; V. Torbidoni, None.
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 3575. doi:
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      A.M. Suburo, V. Torbidoni; Vascular and Glial Changes in Early Stages of Light-Induced Retinal Degeneration . Invest. Ophthalmol. Vis. Sci. 2003;44(13):3575.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract: : Purpose: We have investigated the presence of vascular and glial changes in early stages of retinal degeneration induced to continuous illumination. Methods: BALB-c mice were exposed to 1,500 lux for 1, 3 or 6 days, euthanized and fixed for immunohistochemical and morphometric analyses. Changes in the relationship between retinal arteries and glial cell processes were studied with immunohistochemistry for smooth muscle actin (SMA), glial fibrillary acidic protein (GFAP), endothelin-1 (ET-1) and glutamine synthase (GS). Diameters of radial branches of the retinal artery were measured in retinal wholemounts stained for NADPH-diaphorase activity. Results: Under these illumination conditions a decrease in the thickness of the outer nuclear layer became apparent after 6 days. No modifications of other nuclear layers were detected during this period. In normal retinas, GFAP immunoreactivity was only present in astrocytes. At difference with brain astrocytes, which only express ET-1 after activation, normal retinal astrocytes always exhibited strong ET-1 immunoreactivity. In animals submitted to continuous illumination, GFAP immunoreactivity also appeared in Müller cells. These cells, however, could be recognized by GS immunoreactivity, whereas astrocytes could be identified by ET-1 labeling. Marked astrocytic changes appeared in 3-day illuminated retinas. As demonstrated by ET-1 immunoreactivity, these changes included an increase in the complexity of the astrocytic plexus and a larger number of astrocytic processes surrounding the smooth muscle layer of retinal arterioles. By contrast, no significant differences in the association of Müller cell end-feet with arterioles could be detected in illuminated retinas. Measurement of arterioles demonstrated significant decreases of their diameters after only 3 days of illumination. A reduction in arteriolar diameter was still present in 6-day-illuminated retinas. Conclusions: Continuous illumination induced a strong vasospasm before a decrease in the outer nuclear layer could be detected. Vascular constriction seemed to be related with changes in the relationship between astrocytic processes and the arteriolar wall. Since astrocytic processes express strong ET-1 immunoreactivity, vasospasm could perhaps be explained by an increase in endothelin release. Vasoconstriction probably reduces retinal blood flow and might have a potentiating effect on retinal light-induced injury.

Keywords: retinal glia • retinal degenerations: cell biology • blood supply 

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