Purpose. Choroidal neovascularization (CNV) is the major cause of severe visual loss in patients with age-related macular degeneration. Laser treatment is helpful for only a small minority of patients with CNV and development of new treatment is hampered by a poor understanding of its pathogenesis. Current models of CNV have provided some descriptive information, but they are not amenable to investigation of the role of specific genes; this would be possible in a mouse model which could be used in transgenic mice or mice with a gene knockout. Therefore, in this study we sought to produce and characterize a mouse model of CNV. Methods. Adult C57B6/6J mice were anesthetized and pupils were dilated with 1% tropicamide. Three burns of krypton laser photocoagulation (LPC); 50 μm, 0.05 seconds, 350-400 mW) were delivered to each retina using a slit lamp delivery system and a cover slip as a contact lens. Color fundus photographs and fluorescein angiograms (FAs) were done at various time points (0, 3, 7, 14, or 28 days) immediately prior to sacrifice, after which eyes were enucleated and processed for light and electron microscopy. Results. A central bubble, suggesting rupture of Bruch's membrane, was observed for 67 (89%) of 75 burns in 25 eyes. FAs 1 week after laser showed late leakage from 57% or 64% of all burns or burns which produced a bubble, respectively. CNV was identified by light microscopy in 83% of laser burns. Burns that showed intense leakage by FA had an associated serous retinal detachment. Electron microscopy showed fenetrated vessels with large lumens within CNV lesions. Conclusions. Laser-induced CNV in the mouse provides a highly reproducible model that will be an asset for investigations of the pathogenesis and treatment of CNV.
|Original language||English (US)|
|Journal||Investigative Ophthalmology and Visual Science|
|State||Published - Feb 15 1996|
ASJC Scopus subject areas
- Sensory Systems
- Cellular and Molecular Neuroscience