Abstract
Background: Nerve impulses that are generated in injured nociceptive fibers and enter the spinal cord are known to cause central sensitization leading to neuropathic pain. Injury-induced impulses that are transmitted antidromically into the peripheral terminals of nociceptive fibers may also cause nociceptors to be sensitized, thus contributing to neuropathic pain. However, this possibility has not yet been tested. The present study was designed to investigate the effects of antidromic impulses on the mechanical allodynic behavior seen in a rat model of neuropathic pain. Methods: Male Sprague-Dawley rats were assigned randomly into one of two groups, i.e., a capsaicin group or a vehicle group. Capsaicin group animals were treated with 1% capsaicin (4) in the stump of the distal nerve after severing the fifth left lumbar spinal nerve in order to inhibit delayed and continued antidromic impulses. The vehicle group was treated with same solution without capsaicin. The withdrawal threshold for mechanical allodynia was measured using von Frey hairs in terms of the bending force required to elicit hind-paw withdrawal. Threshold values were compared between the two groups. Results: The capsaicin group showed a statistically significant difference in terms of the paw withdrawal threshold as compared with the corresponding control from 12 days and this remained so until 32 days after treatment. Conclusions: Our results suggest that antidromic impulses developed by nerve injury are partly responsible for the development of mechanical allodynia.
Published Version
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