DELAYED AND SELECTIVE MOTOR-NEURON DEATH AFTER TRANSIENT SPINAL-CORD ISCHEMIA - A ROLE OF APOPTOSIS

Objective: The mechanism of spinal cord injury has been thought to be related to tissue ischemia, and spinal motor neuron cells are suggeste d to be vulnerable to ischemia, We hypothesized that delayed and selec tive motor neuron death is apoptosis, Methods: Thirty-seven Japanese d omesticated white rabbits weighing 2 to 3 kg were used in this study a nd were divided into two subgroups: a 15-minute ischemia group and a s ham control group. Animals were allowed to recover at ambient temperat ure and were killed at 8 hours, and 1, 2, 4, and 7 days after reperfus ion (n = 3 at each time point). By means of this model, cell damage wa s histologically analyzed, Detection of ladders of oligonucleosomal DN A fragment was investigated with gel electrophoresis up to 7 days of t he reperfusion, Immunocytochemistry, in situ terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick-end labeli ng staining was also performed, Results: After 15 minutes of ischemia, most of the motor neurons showed selective cell death at 7 days of re perfusion. Typical ladders of oligonucleosomal DNA fragments were dete cted at 2 days of reperfusion, Immunocytochemistry showed in situ term inal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-b iotin nick-end staining was detected at 2 days of reperfusion selectiv ely in the nuclei of motor neurons. Conclusion: These results suggest that delayed and selective death of the motor neuron cells after trans ient ischemia may not be necrotic but rather predominantly apoptotic.