OBJECTIVE To elucidate the effect of neurotoxin, excitatory amino acid and neuropeptide on spinal cord injury post trauma. METHODS We detected the changes of concentration of EAA, glutamate(Glu) and aspartate(Asp) at injured segment tissue after spinal cord injury. Changes in dynorphin DynA1-13, an endogenous opioid, immnoreactivity following traumatic spinal cord injury in the rat were examined. We observed the effects of Glu and dynorphin DynA1-13 administered intrathecally on function of spinal cord in rats and the effects of 3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid (CPP), an antagonist of EAA receptor, and antisera against dynorphin administered intrathecally on secondary spinal cord injury. RESULTS The concentrations of EAA and dynorphin DynA1-13 increased progressively along with the severity of injury, and were related to injury time. Glu exacerbated the extent of spinal cord injury. Dynorphin DynA1-13 administered intrathecally caused dose-related hindlimb paraplysis in rats, whereas CPP and antisera against dynorphin DynA1-13 were found to have protective effect on spinal cord injury. CONCLUSIONS These findings further support the potential pathophysiological role of EAA and dynorphin DynA1-13 as neurotoxin in spinal cord injury.