CELL-DEATH IN CLARKE COLUMN AFTER SPINAL-CORD TRANSECTION

The death of embryonic CNS neurons deprived of a target is well established. In adult rats, similar cell death of corticospinal and rubrospinal motor neurons occurs as a delayed response to spinal cord transection. The loss of neurons in Clarke''s column, secondary ascending spinocerebellar neurons in adult rats, after complete spinal cord transection at [thoracic] T-9 is documented. After spinal cord transection (25 wk) horseradish peroxidase (HRP) studies showed a dramatic loss of labeled cells in rats with transected spinal cords as compared to matched control rats. Cresyl echt violet-stained sections failed to support the hypothesis that unlabeled cells persist in a shrunken, inactive state; instead far fewer identifiable neurons in Clarke''s column were found. Although little gliosis was seen in the area of cell loss, gliosis was evident in the adjacent corticospinal tract which was severed in the original surgical injury. Amputation of the right hind limb resulted in a paradoxical increase in labeled Clarke''s column cells on the right. Total cells stained with cresyl echt violet in amputated animals were not different from right to left. The increase in labeled cells on the amputated side may have been caused by an increase in metabolic activity of these deafferentated neurons which resulted in more effective axoplasmic transport of the HRP label.