Purpose. To explore the effects of N-methyl-D-aspartate (NMDA) toxicity and retinal ischemia in the neuronal nitric oxide synthase deficient (nNOS-) mouse. Methods. The nNOS- mouse and a control cohort were subjected to (a) intravitreal injections of N-methyl-D-aspartate, or (b) multiple retinal arterial occlusions induced either by thermal photocoagulation or photo-thrombosis. Retinal ganglion cell (RGC) survival was evaluated by retrograde transport of HRP and stereological analysis of retinal whole mounts. Results. nNOS- retinas had fewer RGCs, but preliminary results indicate that this difference was not significant. In the wild type mouse, 63% of the retinal ganglion cells were killed by a single injection of 10 nmol of NMDAr In comparison, only 35% of the NOS-knockout RGC's were lost at this dose. Furthermore, with either retinal arterial occlusion model, the NOS-knockout mouse lost only half as many RGCs as the wild type mouse. Conclusions. These data indicate that the presence of neuronal NOS is a pre-requisite for the full expression of either NMDA retinal excitotoxicity, or of arterial occlusion-mediated RGC loss.
|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