Neuronal nitric oxide synthase is necessary for the full expression of excitotoxicity in the retina

S. H. Yoo, C. K. Vorwerk, J. W. Miller, D. Husain, E. B. Dreyer

Research output: Contribution to journalArticlepeer-review


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 languageEnglish (US)
Pages (from-to)S827
JournalInvestigative Ophthalmology and Visual Science
Issue number3
StatePublished - Feb 15 1996
Externally publishedYes

ASJC Scopus subject areas

  • Ophthalmology
  • Sensory Systems
  • Cellular and Molecular Neuroscience


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