The Role of the Peripheral Chemokine, CCL3, in Hyperalgesia following Peripheral Nerve Injury in the Rat.
10.3344/kjp.2008.21.3.187
- Author:
Joong Woo LEEM
1
;
Hyun Joo LEE
;
Taick Sang NAM
;
Duck Mi YOON
Author Information
1. Department of Physiology, Yonsei University Medical College, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
CCL3;
chemokine;
hyperalgesia;
neuropathic pain;
spinal nerve injury
- MeSH:
Animals;
Axons;
Chemokine CCL3;
Chemokine CCL5;
Diagnosis-Related Groups;
Ganglia, Spinal;
Hyperalgesia;
Ligation;
Neuralgia;
Nociceptors;
Peripheral Nerve Injuries;
Peripheral Nerves;
Rats;
Receptors, CCR1;
Sciatic Nerve;
Skin;
Spinal Nerves;
Up-Regulation;
Wallerian Degeneration
- From:The Korean Journal of Pain
2008;21(3):187-196
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Upregulation of one type of the pro-inflammatory chemokine (CCL2) and its receptor (CCR2) following peripheral nerve injury contributes to the induction of neuropathic pain. Here, we examined whether another type of chemokine (CCL3) is involved in neuropathic pain. METHODS: We measured changes in mechanical and thermal sensitivity in the hind paws of naive rats or rats with an L5 spinal nerve ligation (SNL) after intra-plantar injection of CCL3 or met-RANTES, an antagonist of the CCL3 receptor, CCR1. We also measured CCL3 levels in the sciatic nerve and the hind paw skin as well as CCR1 expression in dorsal root ganglion (DRG) cells from the lumbar spinal segments. RESULTS: Intra-plantar injection of CCL3 into the hind paw of naive rats mimicked L5 SNL-produced hyperalgesia. Intra-plantar injection of met-RANTES into the hind paw of rats with L5 SNL attenuated hyperalgesia. L5 SNL increased CCL3 levels in the sciatic nerve and the hind paw skin on the affected side. The number of CCR1-positive DRG cells in the lumbar segments was not changed following L5 SNL. CONCLUSIONS: Partial peripheral nerve injury increases local CCL3 levels along the degenerating axons during Wallerian degeneration. This CCL3 binds to its receptor, CCR1, located on adjacent uninjured afferents, presumably nociceptors, to induce hyperalgesia in the neuropathic pain state.
