INTACT NOCICEPTION-INDUCED NEUROPLASTICITY IN TRANSGENIC MICE DEFICIENT IN NEURONAL NITRIC-OXIDE SYNTHASE

Nitric oxide is thought to play an important role in multiple forms of use-dependent synaptic plasticity, including that which follows noxio us peripheral stimulation. This suggests that development of nocicepti on-induced neuroplasticity should be impaired in transgenic animals la cking the neuronal form of nitric oxide synthase. We used the formalin model of nociception to test this hypothesis in wild-type and nitric oxide synthase knockout mice. Formalin-induced nociceptive behavior wa s intact in the knockout mice. Furthermore, administration of a nitric oxide synthase inhibitor blocked nociception-induced neuroplasticity in wildtype mice but had no effect in the knockouts, whereas inhalatio n of the gaseous analgesic nitrous oxide attenuated development of neu roplastic changes in both phenotypes. These data indicate that nitric oxide is sufficient but not essential for development of nociception-i nduced neuroplasticity.