PMID- 15041200
OWN - NLM
STAT- MEDLINE
DCOM- 20040512
LR  - 20061115
IS  - 0168-0102 (Print)
IS  - 0168-0102 (Linking)
VI  - 48
IP  - 4
DP  - 2004 Apr
TI  - Enhanced production of monocyte chemoattractant protein-1 in the dorsal root 
      ganglia in a rat model of neuropathic pain: possible involvement in the 
      development of neuropathic pain.
PG  - 463-9
AB  - Chemokines are a family of peptides originally identified as the factors 
      regulating the migration of leukocytes in inflammatory and immune responses. 
      Recently, they have been shown to be produced in the central and peripheral 
      nervous systems under various pathological conditions and act on neuronal and 
      glial cells. In this study, we examined the production of monocyte 
      chemoattractant protein-1 (MCP-1), a well-characterized chemokine, in dorsal root 
      ganglia (DRG) in a rat model of neuropathic pain. Partial ligation of the sciatic 
      nerve induced mechanical allodynia in the ipsilateral hindpaw with weaker 
      allodynia in the contralateral one. Immunohistochemical analyses revealed that 
      the number of MCP-1 immunoreactivity (ir)-positive cells was increased in the 
      ipsilateral DRG. The increase started by 4h after the ligation, peaked at 24h and 
      continued to at least 48 h. The weaker but significant increase was observed in 
      the contralateral DRG. Double immunofluorescent staining demonstrated that almost 
      all of the MCP-1ir-positive cells were neuronal cells. In situ hybridization 
      histochemistry showed that MCP-1 mRNA expression was markedly upregulated in the 
      ipsilateral DRG with weaker increase in the contralateral one at 24 h after the 
      ligation, indicating that the elevation in MCP-1ir detected by 
      immunohistochemistry was due to an upregulation of MCP-1 production by the DRG 
      neurons themselves. Furthermore, intrathecal administration of MCP-1 induced 
      mechanical allodynia. These results suggest that MCP-1 produced in the DRG 
      neurons is involved in the development of mechanical allodynia induced by nerve 
      injury.
FAU - Tanaka, Takahiro
AU  - Tanaka T
AD  - Department of Molecular Pharmacology, Graduate School of Pharmaceutical Sciences, 
      Kyoto University, Kyoto 606-8501, Japan.
FAU - Minami, Masabumi
AU  - Minami M
FAU - Nakagawa, Takayuki
AU  - Nakagawa T
FAU - Satoh, Masamichi
AU  - Satoh M
LA  - eng
PT  - Journal Article
PL  - Ireland
TA  - Neurosci Res
JT  - Neuroscience research
JID - 8500749
RN  - 0 (Chemokine CCL2)
RN  - 0 (RNA, Messenger)
SB  - IM
MH  - Animals
MH  - Chemokine CCL2/administration & dosage/*biosynthesis
MH  - Disease Models, Animal
MH  - Functional Laterality
MH  - Ganglia, Spinal/*metabolism
MH  - Hindlimb/innervation
MH  - Immunohistochemistry
MH  - In Situ Hybridization
MH  - Injections, Spinal
MH  - Ligation
MH  - Male
MH  - Pain/chemically induced/*physiopathology
MH  - RNA, Messenger/analysis
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Sciatic Nerve/injuries
EDAT- 2004/03/26 05:00
MHDA- 2004/05/13 05:00
CRDT- 2004/03/26 05:00
PHST- 2003/11/29 00:00 [received]
PHST- 2004/01/06 00:00 [accepted]
PHST- 2004/03/26 05:00 [pubmed]
PHST- 2004/05/13 05:00 [medline]
PHST- 2004/03/26 05:00 [entrez]
AID - S0168010204000070 [pii]
AID - 10.1016/j.neures.2004.01.004 [doi]
PST - ppublish
SO  - Neurosci Res. 2004 Apr;48(4):463-9. doi: 10.1016/j.neures.2004.01.004.