J Korean Pain Soc.  2003 Jun;16(1):14-22.

Effect of Antidromic Impulses on the Mechanical Allodynia in a Rat Model of Peripheral Neuropathic Pain

• Shin JW
• Hahm KD
• Leem JW
• Park SH
• Choi Y
• Jung WS
• Lee C

Abstract

BACKGROUND
Nerve impulses that are transmitted, antidromically, into peripheral terminals, following nerve injury, may be a factor in neuropathic pain. 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 divided into 5 drug-treated groups; bupivacaine (BUP group), a substance P receptor antagonist; L733060 (SPAL group), a [D-Arg, D-Phe, D-Trp, Leu]- substance P (SPAD group), a calcitonin gene-related peptide receptor antagonist (CGA group) and indomethacin (IND group). The neuropathic pain was induced by tight ligation of the fifth and sixth left spinal nerves. In the BUP group, bupivacaine and normal saline were injected subcutaneously, into the plantar surface of the left hind paw and the back, respectively. In the control group, normal saline and bupivacaine were injected by reversed methods. In the SPAL, SPAD, CGA and IND groups, the active drugs and normal saline were injected subcutaneously, into the plantar surface of the left hind paw and the back, respectively. In the control group, the normal saline and active drug were injected by reversed methods. The withdrawal threshold was measured with von Frey hairs. RESULTS: In the BUP group, the withdrawal threshold increased on days 1, 2 and 3 post-injury. In the CGA group, the CGRP antagonist injection increased the withdrawal thresholds after 15 min, through to 90 min, post-injection. In the IND group, the indomethacin injection reversed the withdrawal threshold at 30 min, through to 120 min, post-injection. However, the SPAL and SPAD group showed no changes compared with the corresponding controls. CONCLUSIONS: The antidromic impulses generated by nerve injury are at least partly responsible for the development of mechanical allodynia, from considering the results of the experiments with bupivacaine. The peripheral neurogenic inflammation produced by antidromic impulses is also partly responsible for the development of mechanical allodynia, according to the results of the experiments with indomethacin and CGRP, of the neurotransmitters released by the antidromic impulses at the peripheral site, is probably more important than SP in the development of mechanical allodynia.

Keyword

Antidromic impulse; Bupivacaine; Calcitonin gene-related peptide; Indomethacin; Neuropathic pain; Substance P

MeSH Terms

Action Potentials
Animals
Bupivacaine
Calcitonin Gene-Related Peptide
Hair
Humans
Hyperalgesia*
Indomethacin
Ligation
Male
Models, Animal*
Neuralgia*
Neurogenic Inflammation
Neurotransmitter Agents
Rats*
Rats, Sprague-Dawley
Receptors, Neurokinin-1
Spinal Nerves
Substance P
Bupivacaine
Calcitonin Gene-Related Peptide
Indomethacin
Neurotransmitter Agents
Receptors, Neurokinin-1
Substance P