Premium
Spinal glial modulation of neuropathic pain using a Spared Nerve Injury model in the mouse
Author(s) -
Nguyen Thao,
Vallejo Ricardo,
Benyamin Ramsin,
Kramer Jeffery,
Vogel Laura A.
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.665.10
Subject(s) - neuropathic pain , medicine , allodynia , anesthesia , sni , nerve injury , microglia , hyperalgesia , spinal nerve , peripheral nerve injury , spinal cord , pharmacology , inflammation , nociception , sciatic nerve , receptor , biochemistry , chemistry , psychiatry , hydrolysis , acid hydrolysis
Neuropathic pain presents a clinical challenge because there are few optimal therapeutic treatments available. The mechanisms of neuropathic pain must be elucidated to provide a foundation for improved pain therapy. Recent evidence implicates spinal cord microglia as a potential cellular modulator of neuropathic pain. We hypothesized that inhibiting microglial activation would decrease pro‐inflammatory cytokine production and alter the neuropathic pain symptom of allodynia in animals with peripheral nerve injury. Animals were treated with propentofylline (PPF; 10 mg/kg/day intraperitoneal injection), an inhibitor of microglial activation, or saline for 14 days starting on day 0. On day 7, animals underwent a sham surgery or Spared Nerve Injury (SNI). Spontaneous pain and cold allodynia behaviors were measured on multiple days post‐surgery. On day 14, lumbar spinal cord tissue was harvested for molecular analysis. RT‐PCR was performed to measure mRNA levels of pro‐inflammatory cytokines TNF‐α and IL‐6 and the microglial activation marker ITGAM. Expression levels of ITGAM, TNF‐α and IL‐6 were decreased in animals administered with PPF. Likewise, spontaneous pain and cold allodynia were attenuated for PPF‐treated animals. The effect of propentofylline on neuropathic pain appears to be a potential tool to examine the mechanism for neuropathic pain. Funded by the Millennium Pain Center.