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 noxious peripheral stimulation. This suggests that development of nociception-induced neuroplasticity should be impaired in transgenic animals lacking 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 was intact in the knockout mice. Furthermore, administration of a nitric oxide synthase inhibitor blocked nociception-induced neuroplasticity in wild-type mice but had no effect in the knockouts, whereas inhalation of the gaseous analgesic nitrous oxide attenuated development of neuroplastic changes in both phenotypes. These data indicate that nitric oxide is sufficient but not essential for development of nociception-induced neuroplasticity.
Crosby
G
G
Department of Anesthesia, Massachusetts General Hospital and Harvard Medical School, Boston 02114, USA.
Marota
J J
JJ
Huang
P L
PL
D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives / Q000494:pharmacology; D051379:Mice; D008822:Mice, Transgenic; D019331:NG-Nitroarginine Methyl Ester; D009473:Neuronal Plasticity / Q000502:physiology*; D009569:Nitric Oxide / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000378:metabolism*; D009609:Nitrous Oxide / Q000494:pharmacology; D010147:Pain Measurement; D013997:Time Factors
D009569:Nitric Oxide; D001120:Arginine; D019001:Nitric Oxide Synthase; D009609:Nitrous Oxide; D019331:NG-Nitroarginine Methyl Ester