PMID- 15464762
OWN - NLM
STAT- MEDLINE
DCOM- 20050106
LR  - 20071114
IS  - 0006-8993 (Print)
IS  - 0006-8993 (Linking)
VI  - 1025
IP  - 1-2
DP  - 2004 Oct 29
TI  - Immunocytochemical localization of TNF type 1 and type 2 receptors in the rat 
      spinal cord.
PG  - 210-9
AB  - Tumor necrosis factor-alpha (TNF-alpha) is secreted in numerous 
      pathophysiological situations by a variety of cell types. Tactile 
      hypersensitivity (allodynia) is one component of a constellation of "illness 
      behaviors" triggered by TNF-alpha. TNF-alpha is also implicated in neuropathic 
      pain after peripheral nerve injury and apoptosis after spinal cord injury (SCI). 
      It is possible that SCI, illness- and peripheral injury-induced hypersensitivity 
      may share a similar spinal mediated etiology. These studies identify the locus of 
      type-1 TNF (TNFR1 or p55) and type-2 TNF (TNFR2 or p75) receptors within the 
      spinal cord. At all spinal levels, TNFR1 receptor immunoreactivity (TNFR1-ir) was 
      constitutively expressed on cells and afferent fibers within the dorsal root 
      ganglia, afferent fibers of the dorsal root, dorsal root entry zone (REZ) and 
      within lamina I and II of the dorsal horn. Unilateral dorsal rhizotomy eliminated 
      the characteristic pattern of TNFR1-ir at the rhizotomized REZ. In contrast, 
      TNFR2-ir was consistently absent from dorsal root fibers and the region of the 
      root entry zone. Consistent with our previous report, medullary afferent fibers 
      in the solitary tract and spinal trigeminal tract labelled for TNF1-ir, but did 
      not express TNFR2-ir. The presence TNFR1-ir on dorsal horn afferents, suggests 
      that TNF-alpha may be a mechanism responsible for tactile hypersensitivity during 
      illness. The presence of TNFR1 receptors, and perhaps their long-term activation 
      or plasticity, may also play a critical role in the chronic allodynia and 
      hyperreflexia observed after SCI or peripheral nerve damage.
FAU - Holmes, Gregory M
AU  - Holmes GM
AD  - Laboratory of Autonomic Neuroscience, Pennington Biomedical Research Center, 6400 
      Perkins Road, Louisiana State University, Baton Rouge, LA 70808, USA. 
      HolmesGM@pbrc.edu
FAU - Hebert, Sadie L
AU  - Hebert SL
FAU - Rogers, Richard C
AU  - Rogers RC
FAU - Hermann, Gerlinda E
AU  - Hermann GE
LA  - eng
GR  - DK 52412/DK/NIDDK NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Netherlands
TA  - Brain Res
JT  - Brain research
JID - 0045503
RN  - 0 (Receptors, Tumor Necrosis Factor, Type I)
RN  - 0 (Receptors, Tumor Necrosis Factor, Type II)
SB  - IM
MH  - Animals
MH  - Female
MH  - Ganglia, Spinal/chemistry/injuries/metabolism
MH  - Immunohistochemistry
MH  - Male
MH  - Rats
MH  - Rats, Long-Evans
MH  - Receptors, Tumor Necrosis Factor, Type I/*analysis/biosynthesis
MH  - Receptors, Tumor Necrosis Factor, Type II/*analysis/biosynthesis
MH  - Spinal Cord/*chemistry/metabolism
EDAT- 2004/10/07 09:00
MHDA- 2005/01/07 09:00
CRDT- 2004/10/07 09:00
PHST- 2004/08/10 00:00 [accepted]
PHST- 2004/10/07 09:00 [pubmed]
PHST- 2005/01/07 09:00 [medline]
PHST- 2004/10/07 09:00 [entrez]
AID - S0006-8993(04)01339-3 [pii]
AID - 10.1016/j.brainres.2004.08.020 [doi]
PST - ppublish
SO  - Brain Res. 2004 Oct 29;1025(1-2):210-9. doi: 10.1016/j.brainres.2004.08.020.