December 1992
Volume 33, Issue 13
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Articles  |   December 1992
GM1 reduces injury-induced metabolic deficits and degeneration in the rat optic nerve.
Author Affiliations
  • E Yoles
    Department of Neurobiology, Weizmann Institute of Science, Rehovot, Israel.
  • M Zalish
    Department of Neurobiology, Weizmann Institute of Science, Rehovot, Israel.
  • V Lavie
    Department of Neurobiology, Weizmann Institute of Science, Rehovot, Israel.
  • R Duvdevani
    Department of Neurobiology, Weizmann Institute of Science, Rehovot, Israel.
  • S Ben-Bassat
    Department of Neurobiology, Weizmann Institute of Science, Rehovot, Israel.
  • M Schwartz
    Department of Neurobiology, Weizmann Institute of Science, Rehovot, Israel.
Investigative Ophthalmology & Visual Science December 1992, Vol.33, 3586-3591. doi:
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    • Get Citation

      E Yoles, M Zalish, V Lavie, R Duvdevani, S Ben-Bassat, M Schwartz; GM1 reduces injury-induced metabolic deficits and degeneration in the rat optic nerve.. Invest. Ophthalmol. Vis. Sci. 1992;33(13):3586-3591.

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

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Abstract

This study demonstrates the earliest reported effects of GM1 treatment on crush-injured axons of the mammalian optic nerve. GM1, administered intraperitoneally immediately after injury, was found to reduce the injury-induced metabolic deficit in nerve activity within 2 hr of injury, as measured by changes in the nicotine-amine adenine dinucleotide redox state. After 4 wk, transmission electron microscopy 1 mm distal to the site of injury revealed a sevenfold increase in axonal survival in GM1-treated compared to untreated injured nerves. These results emphasize the beneficial effect of GM1 on injured optic nerves as well as the correlation between immediate and long-term consequences of the injury. Thus, these results have implications for treating damaged optic nerves.

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