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Article type: Research Article
Authors: Vorwerk, Christian K.; | Bonheur, Jennifer | Kreutz, Michael R. | Dreyer, Evan B. | Laev, Heljo
Affiliations: Department of Ophthalmology, Veterans Administration and the University of Pennsylvania, Philadelphia, PA 19104 USA | AG Mol. & Cellular Neurobiology, Institute of Medical Psychology, Otto von Guericke University and Department of Neurochemistry/ Molecular Biology, Leibniz-Institute for Neurobiology, 39118 Magdeburg, Germany | Division of Neuroscience, New York State Psychiatric Institute and College of Physicians and Surgeons, Columbia University, New York, NY 10032 USA
Abstract: Injury of the nervous system initiates a cascade of signal transduction including a rise in extracellular glutamate which leads to subsequent secondary neuronal loss. Excitotoxicity is known to play a crucial role in cell death spinal cord trauma. Gangliosides, particularly monosialogangliosides (GM1), are protective against various neurological insults, including excitotoxicity. Gangliosides may improve outcome following human spinal cord injury in humans. To further explore the relationship between excitotoxicity and GM1, dissociated murine spinal cord preparations were exposed to glutamate (0.5 mM) with the subsequent administration of GM1 (80 µM) at 8 and 13 days in culture. The addition of GM1 30 minutes after exposure to glumatate significantly reduced neuronal damage and preserved membrane structure and integrity. These results demonstrate that post-treatment with GM1 gangliosides after glutamate-induced excitotoxicity is effective in protecting spinal cord neurons.
Keywords: ganglioside, glutamate, spinal cord, in vitro, LDH, immunohistochemistry
Journal: Restorative Neurology and Neuroscience, vol. 14, no. 1, pp. 47-51, 1999
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