PMID- 15893583
OWN - NLM
STAT- MEDLINE
DCOM- 20050802
LR  - 20131121
IS  - 0169-328X (Print)
IS  - 0169-328X (Linking)
VI  - 136
IP  - 1-2
DP  - 2005 May 20
TI  - Contralateral cytokine gene induction after peripheral nerve lesions: dependence 
      on the mode of injury and NMDA receptor signaling.
PG  - 23-8
AB  - There is increasing evidence that unilateral nerve injury evokes contralateral 
      responses, but the underlying mechanisms are largely unknown. In the present 
      investigation, we analyzed cytokine and chemokine gene induction in 
      contralateral, non-lesioned nerves after sciatic nerve crush and chronic 
      constriction injury (CCI) by quantitative reverse transcriptase polymerase chain 
      reaction in mice. After sciatic nerve crush, contralateral changes in cytokine 
      gene expression were restricted to interleukin (IL)-1beta, which showed a 
      monophasic peak at the first postoperative day. Following CCI, contralateral 
      transcripts for IL-1beta, IL-10 and monocyte chemoattractant protein-1 (MCP-1) 
      were significantly increased already at day 1 and upregulation persisted over the 
      next 4 weeks. In contrast, tumor necrosis factor alpha (TNF-alpha) levels 
      remained unchanged. Contralateral gene induction was restricted to the homonymous 
      opposite sciatic nerve, but spared the femoral nerve. NMDA receptor blockade 
      completely abolished contralateral cytokine expression after CCI on the mRNA 
      level. In contralateral dorsal root ganglia, only IL-10 mRNA levels were modified 
      after nerve injury. Sham operation significantly increased the cytokine and 
      chemokine gene expression at the ipsilateral side, but could not mediate 
      contralateral effects. Our study confirms that nerve injury evokes contralateral 
      responses and identifies NMDA-mediated signaling as one underlying mechanism.
FAU - Kleinschnitz, C
AU  - Kleinschnitz C
AD  - Department of Neurology, Julius-Maximilians Universitat, Josef-Schneider-Str. 11, 
      D-97080 Wurzburg, Germany.
FAU - Brinkhoff, J
AU  - Brinkhoff J
FAU - Sommer, C
AU  - Sommer C
FAU - Stoll, G
AU  - Stoll G
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - Brain Res Mol Brain Res
JT  - Brain research. Molecular brain research
JID - 8908640
RN  - 0 (Chemokines)
RN  - 0 (Cytokines)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 6LR8C1B66Q (Dizocilpine Maleate)
SB  - IM
MH  - Analysis of Variance
MH  - Animals
MH  - Chemokines/genetics/metabolism
MH  - Cytokines/genetics/*metabolism
MH  - Disease Models, Animal
MH  - Dizocilpine Maleate
MH  - Female
MH  - Functional Laterality/*physiology
MH  - Gene Expression/physiology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Nerve Crush/methods
MH  - Peripheral Nervous System Diseases/*metabolism
MH  - RNA, Messenger/biosynthesis
MH  - Receptors, N-Methyl-D-Aspartate/*physiology
MH  - Reverse Transcriptase Polymerase Chain Reaction/methods
MH  - Sciatic Neuropathy/metabolism
MH  - Time Factors
EDAT- 2005/05/17 09:00
MHDA- 2005/08/03 09:00
CRDT- 2005/05/17 09:00
PHST- 2004/09/27 00:00 [received]
PHST- 2004/12/21 00:00 [revised]
PHST- 2004/12/22 00:00 [accepted]
PHST- 2005/05/17 09:00 [pubmed]
PHST- 2005/08/03 09:00 [medline]
PHST- 2005/05/17 09:00 [entrez]
AID - S0169-328X(05)00002-1 [pii]
AID - 10.1016/j.molbrainres.2004.12.015 [doi]
PST - ppublish
SO  - Brain Res Mol Brain Res. 2005 May 20;136(1-2):23-8. doi: 
      10.1016/j.molbrainres.2004.12.015.