Glutamate Induces Cell Death In The Spinal Cord Without Elevating H2o2, Malondialdehyde Or The Redox State Of The Tissue

Substantial quantities of glutamate and reactive oxygen species are released following neurotraumas. Present work establishes that administering glutamate into the spinal cord at the level at which it is released following spinal cord injury did not significantly change the levels of superoxide or malondialdehyde released, nor did it change the ratio of the concentrations of reduced glutathione to oxidized glutathione, i.e., the redox state of the exposed tissue. Nonetheless, administering into the spinal cord the level of glutamate released by spinal cord injury substantially increased neuron death. Thus mechanisms of glutamate toxicity other than the generation of toxic oxygen species likely mediate the secondary damage that accompanies spinal cord injury.