RT Journal Article
SR Electronic
T1 Neuronal Nitric Oxide Synthase mRNA Upregulation in Rat Sensory Neurons after Spinal Nerve Ligation: Lack of a Role in Allodynia Development
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 9201
OP 9208
DO 10.1523/JNEUROSCI.19-21-09201.1999
VO 19
IS 21
A1 Z. David Luo
A1 S. R. Chaplan
A1 B. P. Scott
A1 D. Cizkova
A1 N. A. Calcutt
A1 T. L. Yaksh
YR 1999
UL http://www.jneurosci.org/content/19/21/9201.abstract
AB Pharmacological evidence suggests a functional role for spinal nitric oxide (NO) in the modulation of thermal and/or inflammatory hyperalgesia. To assess the role of NO in nerve injury-induced tactile allodynia, we examined neuronal NO synthase (nNOS) expression in the spinal cord and dorsal root ganglia (DRG) of rats with tactile allodynia because of either tight ligation of the left fifth and sixth lumbar spinal nerves or streptozotocin-induced diabetic neuropathy. RNase protection assays indicated that nNOS mRNA (1) was upregulated in DRG, but not spinal cord, neurons on the injury side beginning 1 d after nerve ligation, (2) peaked (∼10-fold increase) at 2 d, and (3) remained elevated for at least 13 weeks. A corresponding increase in DRG nNOS protein was also observed and localized principally to small and occasionally medium-size sensory neurons. In rats with diabetic neuropathy, there was no significant change in DRG nNOS mRNA. However, similar increases in DRG nNOS mRNA were observed in rats that did not develop allodynia after nerve ligation and in rats fully recovered from allodynia 3 months after the nerve ligation. Systemic treatment with a specific pharmacological inhibitor of nNOS failed to prevent or reverse allodynia in nerve-injured rats. Thus, regulation of nNOS may contribute to the development of neuronal plasticity after specific types of peripheral nerve injury. However, upregulation of nNOS is not responsible for the development and/or maintenance of allodynia after nerve injury.