Regulation and localization of neuronal nitric oxide synthase in the ischemic rabbit spinal cord.

The expression and cellular localization of neuronal nitric oxide (NO) synthase (nNOS) were studied in the rabbit spinal cord following ischemic injury induced by clamping the descending aorta. In the normal spinal cord, nNOS immunoreactivity was localized to certain motor neurons located in the margin of the ventral horn. Following transient ischemia, immunoreactive spinal neurons increased in number, peaking five days after reperfusion. Quantitative evaluation by western blotting showed that nNOS peaked at 180% of control levels five days after reperfusion and decreased to 120% of controls by 14 days. These findings suggest that overproduced NO may act as a neurotoxic agent in the ischemic spinal cord.