J Korean Pain Soc.
2000 Jun;13(1):19-30.
Effects of NO Synthase Inhibitor on Responsiveness of Dorsal Horn Neurons
in Neuropathic Pain Animal Model
- Affiliations
-
- 1Department of Physiology, Yonsei University College of Medicine, Seoul, Korea.
- 2Department of Anesthesiology, Yonsei University College of Medicine, Seoul, Korea.
Abstract
-
BACKGROUND: Partial nerve injury to a peripheral nerve may induce the development of
neuropathic pain which is characterized by symptams such as spontaneous burning pain,
allodynia and hyperalgesia. Though underlying mechanism has not fully understood,
sensitization of dorsal horn neurons may con- tribute to generate such symptoms. Nitric
oxide acts as an inter- and intracellular messenger in the nervous system and is produced
from L-arginine by nitric oxide synthase (NOS). Evidence is accumulating which indicate
that nitric oxide may mediate nociceptive information trsnsmission. Recently, it has been
reported that NOS inhibitor suppresses neuropathic pain behavior in an neuropathic pain
animal model. This study was conducted to determine whether nitric oxide could be involved
in the sensitization of dorsal horn neurons in neuropathic animal model.
METHODS
Neuropathic animal model was made by tightly ligating the left L5 and L6 spinal
nerves and we examined the effects of iontophoretically applied NOS inhibitot (L-NAME)
on the dorsal horn neurons responses to mechanical stimuli within the receptive fields.
RESULTS
In normal animals, NOS inhibitor (L-NAME) specifically suppressed the responses
to the noxious mechanical stimuli. In neuropathic animals, the dorsal horn neuron's responses
to mechanical stimuli were enhanced and NOS inhibitor suppressed the dorsal horn neurons
enhanced responses to non-noxious stimuli as well as those to noxious ones.
CONCLUSIONS
These results suggest that nitric oxide may mediate nociceptive transmission
in normal animal and also mediate sensitization of dorsal horn neurons in neuropathic pain
state.