Expression of nitric-oxide synthase (NOS) in injured CNS neurons as shown by NADPH diaphorase histochemistry.

Recent studies have implicated nitric oxide (NO) in several mechanisms related to neuronal degeneration and synaptic plasticity. In the present study, two models of traumatic neuronal injury were used to examine the expression of NOS following neuronal injury and its relationship to axonal sprouting and neuronal degeneration. It was found that NOS is induced in a week of axonal injury in neurons that are normally NOS-negative. Spinal motoneurons express the enzyme after ventral root avulsion, but not after ventral root transection. Neurons of the nucleus dorsalis of the spinal cord express NOS after ipsilateral spinal cord hemisection. These two models provide information about the time course of NOS expression in injured neurons and the opportunity in future studies to determine the role of NOS and its product, NO, in CNS injury. Observations from the present study suggest that early NOS expression seems to be associated with axonal sprouting and growth. Interestingly, though, the neurons expressing lesion-induced NOS ultimately die. Whether NOS expression in these cells is related to their death is currently under investigation.