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

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

Research output: Contribution to journalArticle

Abstract

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
JournalInvestigative Ophthalmology and Visual Science
Volume37
Issue number3
StatePublished - Feb 15 1996
Externally publishedYes

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Nitric Oxide Synthase Type I
Retina
Retinal Ganglion Cells
N-Methylaspartate
Intravitreal Injections
Light Coagulation
Knockout Mice
Cell Survival
Thrombosis
Ischemia
Hot Temperature
Injections

ASJC Scopus subject areas

  • Ophthalmology

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Neuronal nitric oxide synthase is necessary for the full expression of excitotoxicity in the retina. / Yoo, Sonia H; Vorwerk, C. K.; Miller, J. W.; Husain, D.; Dreyer, E. B.

In: Investigative Ophthalmology and Visual Science, Vol. 37, No. 3, 15.02.1996.

Research output: Contribution to journalArticle

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abstract = "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.",
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AU - Vorwerk, C. K.

AU - Miller, J. W.

AU - Husain, D.

AU - Dreyer, E. B.

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AB - 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.

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