Nitric Oxide Expression and Regulation in the Dorsal Root Ganglion and Spinal Cord

Nitric oxide (NO), a free-radical gas, has recently received prominence because of its potential roles in neuronal function. Because it is an unstable molecule the study of its biological activity has been largely focused on its synthetic enzyme, nitric oxide synthase (NOS). The gene encoding constitutive brain NOS has recently been identified.'JJs The enzymatic activity of brain NOS is thought to be calmodulindependent and its activation is coupled to N-methy1-D-aspartate (NMDA) receptor mediated Ca2+ influx. Following their discovery of NOS, Bredt and Snyder2 hypothesized a variety of functional roles for nitric oxide (NO). NO may serve as a neuronal messenger. NO may also be involved in protection of neurons from excitotoxic events. Neurons that contain reduced nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d), an enzyme believed to be identical to NOS,3,4 may be resistant to some forms of excitotoxicity and survive neurodegenerative Alternatively, NO itself is highly toxic and may mediate neurotoxicity if an excess amount is produced.' The specific function of NO, however, is largely unknown. To further understand the function of NO and to determine whether the presence of NO was neuroprotective, we examined NOS in the dorsal root ganglion (DRG) and the spinal cord and the response of DRG neurons to nerve injury.