RGD Reference Report - Differences between tumor necrosis factor-alpha receptors types 1 and 2 in the modulation of spinal glial cell activation and mechanical allodynia in a rat sciatic nerve injury model. - Rat Genome Database

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Differences between tumor necrosis factor-alpha receptors types 1 and 2 in the modulation of spinal glial cell activation and mechanical allodynia in a rat sciatic nerve injury model.

Authors: Ishikawa, T  Miyagi, M  Kamoda, H  Orita, S  Eguchi, Y  Arai, G  Suzuki, M  Sakuma, Y  Oikawa, Y  Inoue, G  Aoki, Y  Toyone, T  Takahashi, K  Ohtori, S 
Citation: Ishikawa T, etal., Spine (Phila Pa 1976). 2013 Jan 1;38(1):11-6. doi: 10.1097/BRS.0b013e3182610fa9.
RGD ID: 8661750
Pubmed: PMID:22652595   (View Abstract at PubMed)
DOI: DOI:10.1097/BRS.0b013e3182610fa9   (Journal Full-text)

STUDY DESIGN: Immunohistological analysis of spinal glial cells and analysis of pain behavior in the rat neuropathic pain model were investigated to clarify the function of tumor necrosis factor (TNF)-alpha receptors p55 type 1 and p75 type 2. OBJECTIVE: Our objective was to investigate changes in hyperalgesia and glial cell activation after injection of antibodies to each TNF receptor in a rat sciatic nerve injury model. SUMMARY OF BACKGROUND DATA: Recent research has revealed that activation of spinal glia plays an important role in radicular and neuropathic pain. TNF-alpha is reportedly a modulator for glial cell activation; however, the precise relationship between TNF-alpha and its 2 receptors on glial cells has not been fully delineated. METHODS: Chronic constriction sciatic nerve injury and sham-operated rats were used. Antibodies to p55 or p75 or saline were intrathecally injected at the L5 level into rats with chronic constriction injury. Mechanical allodynia was examined for 2 weeks. Spinal cords were removed for immunohistochemical studies of ionized calcium-binding adaptor molecule 1 or glial fibrillary acidic protein. RESULTS: Saline rats showed significantly more mechanical allodynia and the number of ionized calcium-binding adaptor molecule 1--immunoreactive microglia and glial fibrillary acidic protein--immunoreactive astrocytes were significantly increased in the saline rats compared with sham-operated rats during the 2 weeks. Injection of both antibodies significantly reduced pain behavior and anti-p55 caused significantly greater reduction compared with anti-p75. The numbers of microglia in both the antibodies groups were significantly decreased when compared with the saline group. In addition, the anti-p55 antibody suppressed microglial activation more than the anti-p75 antibody. CONCLUSION: These results indicate that the microglial TNF-alpha p55 pathway played a more important role than the TNF-alpha p75 pathway in the pathogenesis of peripheral nerve injury pain. This suggests that future studies seeking to clarify neuropathic pain should target TNF-alpha and p55 receptors in microglia.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Hyperalgesia  ISOTnfrsf1a (Rattus norvegicus)8661750; 8661750associated with Sciatic NeuropathyRGD 
Hyperalgesia  ISOTnfrsf1b (Rattus norvegicus)8661750; 8661750associated with Sciatic NeuropathyRGD 
Hyperalgesia  IMP 8661750; 8661750associated with Sciatic NeuropathyRGD 

Objects Annotated

Genes (Rattus norvegicus)
Tnfrsf1a  (TNF receptor superfamily member 1A)
Tnfrsf1b  (TNF receptor superfamily member 1B)

Genes (Mus musculus)
Tnfrsf1a  (tumor necrosis factor receptor superfamily, member 1a)
Tnfrsf1b  (tumor necrosis factor receptor superfamily, member 1b)

Genes (Homo sapiens)
TNFRSF1A  (TNF receptor superfamily member 1A)
TNFRSF1B  (TNF receptor superfamily member 1B)


Additional Information