September 1997
Volume 38, Issue 10
Free
Articles  |   September 1997
The role of neuronal and endothelial nitric oxide synthase in retinal excitotoxicity.
Author Affiliations
  • C K Vorwerk
    Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, USA.
  • B T Hyman
    Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, USA.
  • J W Miller
    Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, USA.
  • D Husain
    Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, USA.
  • D Zurakowski
    Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, USA.
  • P L Huang
    Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, USA.
  • M C Fishman
    Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, USA.
  • E B Dreyer
    Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, USA.
Investigative Ophthalmology & Visual Science September 1997, Vol.38, 2038-2044. doi:
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    • Get Citation

      C K Vorwerk, B T Hyman, J W Miller, D Husain, D Zurakowski, P L Huang, M C Fishman, E B Dreyer; The role of neuronal and endothelial nitric oxide synthase in retinal excitotoxicity.. Invest. Ophthalmol. Vis. Sci. 1997;38(10):2038-2044.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

PURPOSE: Nitric oxide synthase (NOS) plays an essential role in neuronal function and is critical in the brain for normal and pathologic responses to glutamate. The role of NOS in the retina is less well understood. The retina provides an experimental system in which the intrinsic circuitry is well defined; retinal excitotoxic damage has been well characterized. METHODS: To determine whether neuronal NOS (nNOS) and endothelial NOS (eNOS) are critical in excitotoxic damage in the retina, nNOS- and eNOS-deficient mice were subjected to intravitreal injections of N-methyl-D-aspartate (NMDA) or to arterial occlusions. RESULTS: Retinal ganglion cells in the nNOS-deficient mouse were relatively resistant to NMDA and to arterial occlusion. In contrast, the damage in the eNOS-deficient mouse retina was not distinguishable from that in control animals. Preinjection with an NOS inhibitor was partially protective. CONCLUSIONS: The presence of nNOS is a prerequisite for the full expression of excitotoxicity in the retina; eNOS does not appear to play a significant role.

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