Ganglion Cell Death in Rat Retinaby Persistent Intraocular Pressure Elevation.
- Author:
Do Hyun KIM
1
;
Hwa Sun KIM
;
Myung Douk AHN
;
Myung Hoon CHUN
Author Information
- Publication Type:Original Article
- Keywords: apoptosis; glaucoma; retinal ganglion cell
- MeSH: Animals; *Apoptosis; Axonal Transport; Disease Models, Animal; In Situ Nick-End Labeling; *Intraocular Pressure; Male; Ocular Hypertension/*complications; Rats; Rats, Sprague-Dawley; Retinal Ganglion Cells/*pathology; Retrograde Degeneration/etiology; Sclera/blood supply
- From:Korean Journal of Ophthalmology 2004;18(1):15-22
- CountryRepublic of Korea
- Language:English
- Abstract: Glaucoma is characterized by loss of retinal ganglion cells (RGCs) and their axons. Retrograde axoplasmic transport blockade and excitotoxicity were proposed to be a major cause of RGC apoptosis. We conducted this study to characterize the episcleral vessel cauterization glaucoma model in the rat with respect to decreased retrograde axoplasmic flow and subsequent apoptotic RGC death. After episcleral vessels were cauterized in Sprague-Dawley rats, Fluorogold was injected into their superior colliculi by stereotactic method. Retrograde axoplasmic flow and TUNEL-stained apoptotic dead cells were observed microscopically. Elevated intraocular pressure was maintained for up to 6 weeks during follow-up. Retrograde axoplasmic flow to the rat retina was significantly decreased. Apoptotic RGC was selectively TUNELstained in the retina, especially at the ganglion cell layers. We concluded that elevated intraocular pressure caused apoptotic RGC death through retrograde axoplasmic flow blockage. Further studies will elucidate the neuroprotection strategies in glaucoma patients.
