The purpose of this study was to examine the effects of inhibiting
ionotropic glutamate receptor subtypes on measures of oxidative stress events at acute times following traumatic
spinal cord injury (SCI). Rats received a moderate
contusion injury and 15 min later were treated with one of two doses of 1,2,3,4-tetrahydro-6-nitro-2,3-dioxo-
benzol[f]
quinoxaline-7-
sulfonamide disodium (
NBQX),
MK-801, or the appropriate vehicle. At 4 h following
injury, spinal cords were removed and a crude synaptosomal preparation obtained to examine mitochondrial function using the MTT assay, as well as measures of
reactive oxygen species (ROS), lipid peroxidation, and
glutamate and
glucose uptake. We report here that intraspinal treatment with either 15 or 30 nmol of
NBQX improves mitochondrial function and reduces the levels of ROS and lipid peroxidation products. In contrast,
MK-801, given intravenously at doses of 1.0 or 5.0 mg/kg, was without effect on these same measures. Neither
drug treatment had an effect on
glutamate or
glucose uptake, both of which are reduced at acute times following SCI. Previous studies have documented that drugs acting on non-
N-methyl-D-aspartate (
NMDA) receptors exhibit greater efficacy compared to
NMDA receptor antagonists on recovery of function and tissue sparing following traumatic
spinal cord injury. The results of this study provide a potential mechanism by which blockade of the non-
NMDA ionotropic receptors exhibit positive effects following traumatic SCI.