AN EXPERIMENTAL-MODEL COMBINING MICRODIALYSIS WITH ELECTROPHYSIOLOGY, HISTOLOGY, AND NEUROCHEMISTRY FOR STUDYING EXCITOTOXICITY IN SPINAL-CORD INJURY - EFFECT OF NMDA AND KAINATE

We used an experimental model that we previously developed to characterize the damage caused by the agonists of glutamate receptors, N-methyl-D-aspartate (NMDA) and kainate, in the spinal cord in vivo, thereby testing further the utility of this model. Microdialysis was used to administer the toxins and to sample the release of other substances in response to these agents. The blockage of electrical conduction was monitored by recording the amplitudes of evoked potentials during administration of the damaging substances, and damage was assessed by postmortem histological examination. The released amino acids in microdialysates were measured by HPLC. Administration of 5 mM NMDA + 5 mM kainate into the gray matter blocked most postsynaptic responses and caused the release of amino acids. Administration of 10 mM NMDA and 10 mM kainate significantly destroyed cell bodies near the fiber. The advantage of this model is that histological, neurochemical, and electrophysiological parameters were obtained in the same experiment.