Evidence that reversed glutamate uptake contributes significantly to glutamate release following experimental injury to the rat spinal cord

Released excitatory amino acids contribute significantly to secondary damag e following spinal cord injury. Reversal of normal transport due to cell me mbrane depolarization may contribute to this release. We tested this by adm inistering dihydrokainic acid (DHK), a non-transported glutamate uptake blo cker, into the rat spinal cord by microdialysis in association with contusi on spinal cord injury. Glutamate release in response to injury was reduced by 34% (P<0.05) when 3 mM DHK was administered within the microdialysis fib er, suggesting that reversed transport is an important contributor to gluta mate release upon spinal cord injury. (C) 2000 Elsevier Science B.V. All ri ghts reserved.