NADPH Diaphorase Expression in the Rat Retina after Axotomy—a Supportive Role for Nitric Oxide?

NADPH Diaphorase Expression in the Rat Retina after Axotomy—a Supportive Role for Nitric Oxide? The large majority of mammalian retinal ganglion cells degenerate following section of their axons in the optic nerve. It has been suggested that some axotomized retinal ganglion cells die because of toxic agents produced within their immediate environment. Our hypothesis was that nitric oxide might be one of the toxic factors implicated in the death of adult retinal ganglion cells post‐axotomy. In the first instance, we determined whether there were any changes in the retinal expression of NADPH diaphorase both 3 and 14 days following intraorbital section of the optic nerve in adult rats. Secondly, if nitric oxide was indeed implicated in the death of ganglion cells, then trophic factors which rescue these neurons might do so by decreasing the expression of nitric oxide synthase. Recently, we found that a collicular proteoglycan purified from the major target of retinal ganglion cells, the superior colliculus, rescued a greater proportion of adult ganglion cells from axotomy‐induced death than most other known trophic factors. We thus injected this proteoglycan intraocularly after section of the optic nerve and examined its effect on the expression of NADPH diaphorase in the retina. Thirdly, an inhibitor of nitric oxide synthetase was repeatedly injected into the eye following the section of the optic nerve in order to determine if such a treatment might improve the survival of retinal ganglion cells. The present results indicate that section of the optic nerve does not alter the overall levels of NADPH diaphorase within the adult rat retina. Intraocular injections of the collicular proteoglycan actually increased the number of neurons expressing NADPH diaphorase, particularly in the ganglion cell layer. Finally, inhibition of nitric oxide synthetase following axotomy resulted in increased loss of retinal ganglion cells over a 2 week period when compared with controls. Our findings indicate that, rather than being toxic, small amounts of nitric oxide may be important for the survival of a proportion of injured retinal ganglion cells. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png European Journal of Neuroscience Wiley

NADPH Diaphorase Expression in the Rat Retina after Axotomy—a Supportive Role for Nitric Oxide?

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Abstract

The large majority of mammalian retinal ganglion cells degenerate following section of their axons in the optic nerve. It has been suggested that some axotomized retinal ganglion cells die because of toxic agents produced within their immediate environment. Our hypothesis was that nitric oxide might be one of the toxic factors implicated in the death of adult retinal ganglion cells post‐axotomy. In the first instance, we determined whether there were any changes in the retinal expression of NADPH diaphorase both 3 and 14 days following intraorbital section of the optic nerve in adult rats. Secondly, if nitric oxide was indeed implicated in the death of ganglion cells, then trophic factors which rescue these neurons might do so by decreasing the expression of nitric oxide synthase. Recently, we found that a collicular proteoglycan purified from the major target of retinal ganglion cells, the superior colliculus, rescued a greater proportion of adult ganglion cells from axotomy‐induced death than most other known trophic factors. We thus injected this proteoglycan intraocularly after section of the optic nerve and examined its effect on the expression of NADPH diaphorase in the retina. Thirdly, an inhibitor of nitric oxide synthetase was repeatedly injected into the eye following the section of the optic nerve in order to determine if such a treatment might improve the survival of retinal ganglion cells. The present results indicate that section of the optic nerve does not alter the overall levels of NADPH diaphorase within the adult rat retina. Intraocular injections of the collicular proteoglycan actually increased the number of neurons expressing NADPH diaphorase, particularly in the ganglion cell layer. Finally, inhibition of nitric oxide synthetase following axotomy resulted in increased loss of retinal ganglion cells over a 2 week period when compared with controls. Our findings indicate that, rather than being toxic, small amounts of nitric oxide may be important for the survival of a proportion of injured retinal ganglion cells.

Journal

European Journal of NeuroscienceWiley

Published: Nov 1, 1995

References

  • Transplant of embryonal nervous tissue preserves the responses of rat retinal ganglion cells after section of the optic nerve
    Gravina, Gravina; Domenici, Domenici; Berardi, Berardi; Galli, Galli; Maffei, Maffei
  • NADPH‐diaphorase expression in neurons and glia of the normal adult rat retina
    Huxlin, Huxlin
  • Effect of collicular proteoglycan on the survival of adult rat retinal ganglion cells following axotomy
    Huxlin, Huxlin; Dreher, Dreher; Schulz, Schulz; Sefton, Sefton; Bennett, Bennett
  • Long term induction of c‐jun mRNA and Jun protein in rabbit retinal ganglion cells following axotomy or colchicine treatment
    Koistinaho, Koistinaho; Hicks, Hicks; Sagar, Sagar
  • A retinal ganglion cell neurotrophic factor purified from the superior colliculus
    Schulz, Schulz; Raju, Raju; Ralston, Ralston; Bennett, Bennett
  • Morphological comparisons between outer and inner ramifying alpha cells of the albino rat retina
    Tauchi, Tauchi; Morigiwa, Morigiwa; Fukuda, Fukuda
  • The relationship of microglial cells to dying neurons during natural neuronal death and axotomy‐induced degeneration of the rat retina
    Thanos, Thanos

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