May 2004
Volume 45, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2004
TRANSIENT ISCHEMIA OF THE RETINA RESULTS IN LOSS OF RETINAL GANGLION CELLS AND A CORRELATED DEGENERATION OF THE RETINOTECTAL INNERVATION. NEUROPROTECTIVE EFFECTS OF TOPICAL BRIMONIDINE.
Author Affiliations & Notes
  • M. Vidal–Sanz
    Ofttalmología, Universidad De Murcia, Murcia, Spain
  • S. Mayor–Torroglosa
    Ofttalmología, Universidad De Murcia, Murcia, Spain
  • M.P. Lafuente
    Ofttalmología, Universidad De Murcia, Murcia, Spain
  • A. García–Avilés
    Ofttalmología, Universidad De Murcia, Murcia, Spain
  • J.M. Bernal
    Ofttalmología, Universidad De Murcia, Murcia, Spain
  • M.P. Villegas–Pérez
    Ofttalmología, Universidad De Murcia, Murcia, Spain
  • Footnotes
    Commercial Relationships  M. Vidal–Sanz, Allergan Inc. F; S. Mayor–Torroglosa, None; M.P. Lafuente, None; A. García–Avilés, None; J.M. Bernal, None; M.P. Villegas–Pérez, None.
  • Footnotes
    Support  PI82/00540/FS/01, BFI2002–03742, PI020407, Allergan Inc.
Investigative Ophthalmology & Visual Science May 2004, Vol.45, 899. doi:
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      M. Vidal–Sanz, S. Mayor–Torroglosa, M.P. Lafuente, A. García–Avilés, J.M. Bernal, M.P. Villegas–Pérez; TRANSIENT ISCHEMIA OF THE RETINA RESULTS IN LOSS OF RETINAL GANGLION CELLS AND A CORRELATED DEGENERATION OF THE RETINOTECTAL INNERVATION. NEUROPROTECTIVE EFFECTS OF TOPICAL BRIMONIDINE. . Invest. Ophthalmol. Vis. Sci. 2004;45(13):899.

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Abstract

Abstract: : Purpose: To study the correlation between retinal ganglion cell (RGC) loss and the reduction of retino–tectal innervation induced by transient ischemia of the retina, and the neuroprotective effects of topical brimonidine. Methods: In female Sprague–Dawley rats (180 g), 90 minutes of ischemia were induced by transient ligature of the left ophthalmic vessels (LOV). One h before ischemia the left eye was treated with two 5µl drops of saline alone (vehicle group) or containing 0,5% brimonidine (BMD group). An additional group of untouched animals were used as controls. To identify the retinotectal projection, cholera toxin subunit B (CTB) was injected in the left eye 4 weeks after LOV. Five days later, the intracranial aspect of the left optic nerve was divided to apply fluorogold (FG) in order to identify by retrograde transport the population of surviving RGCs. Five days later animals were sacrificed, their retinas were flat mounted and FG–labelled RGC densities were estimated in the right control and left experimental retinas of each animal. In addition, the brains were dissected and serial coronal cryostat sections (40 µm thick) of the midbrain were stained for CTB. The extension of areas densely innervated by CTB–labelled RGC terminals in the visual layers of the contralateral superior colliculus (SC) was determined with the aid of an image analysis system to estimate the volume of the retino–tectal projection. Results: In the control group of animals (n=10) the densities of FG–labelled RGCs were 1528 ±321 (mean±SD) and its corresponding retino–tectal innervation occupied a mean volume of 1,69±0.17 mm3. In the vehicle–treated group of animals (n=11) the densities of FG–labelled RGCs had diminished to approximately 20% of the control values and the retino–tectal innervation occupied a mean volume that represented approximately 45% of the control values. In the BMD–treated group of animals (n=9) the densities of FG–labelled RGCs and its corresponding retino–tectal innervation were significantly greater than those obtained in the vehicle–group; these corresponded to 52% and 70%, respectively, of the values obtained in control animals. Conclusions: Retinal ischemia induces 6 weeks later the loss of approximately 80% of the RGC population and this is associated with the loss of 55% of the volume of the retinotectal innervation. Topical BMD resulted in statistically significant protection against ischemia–induced degeneration of RGCs and their main retinofugal projection.

Keywords: neuroprotection • ganglion cells • ischemia 
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