title: Activation of astrocytes and microglia in the C3-T4 dorsal horn by lower trunk avulsion in a rat model of neuropathic pain.
abstract: OBJECTIVE
  Brachial plexus pain is thought to be generated not by avulsed roots but rather by nonavulsed roots, because avulsed roots could not transmit action potentials to central nerves. The aim of this study was to evaluate pain-related behavior and the extent of glial activation in a model of brachial plexus avulsion (BPA).
  
  
  METHODS
  We used 24 male Wistar rats. For rats in the BPA group, the C8-T1 roots were avulsed from the spinal cord at the level of the lower trunk (n = 10). Rats in a sham-surgery group had a similar surgery without the root avulsion (n = 7). Rats in an untreated group had no surgery (n = 7). Mechanical hyperalgesia of the forelimb plantar surfaces corresponding to C6 and C7 dermatomes was evaluated using a Semmes-Weinstein monofilament test every third day for 3 weeks (n = 15). Activation of astrocytes and microglia was examined immunohistochemically using anti-glia fibrillary acidic protein and anti-Iba1 antibodies 3 days after surgery (n = 9).
  
  
  RESULTS
  When compared with rats in the sham-surgery and naive control groups, rats in the BPA group displayed significant mechanical hyperalgesia in the dermatome innervated by uninjured nerves both ipsilaterally and contralaterally and continuing through day 21. Iba1-immunoreactive microglia and glia fibrillary acidic protein-immunoreactive astrocytes were significantly activated on the ipsilateral side in the BPA group from levels C3 to T3 compared with the sham-surgery and untreated groups of rats.
  
  
  CONCLUSIONS
  Activation of glia at uninjured levels of the dorsal horn may facilitate pain transmission following BPA injury. Consequently, spared spinal glial cells may represent therapeutic targets for treatment of pain related to BPA injury.
  
  
  CONCLUSIONS
  Our findings may indicate why neuropathic pain is so frequent and intense following BPA injury.
authors.affiliation: Department of Orthopaedic Surgery, Graduate School of Medicine, Chiba University, Chiba, Japan.
authors.forename: Ryutaro
authors.initials: R
authors.lastname: Iwasaki
authors.forename: Yusuke
authors.initials: Y
authors.lastname: Matsuura
authors.forename: Seiji
authors.initials: S
authors.lastname: Ohtori
authors.forename: Takane
authors.initials: T
authors.lastname: Suzuki
authors.forename: Kazuki
authors.initials: K
authors.lastname: Kuniyoshi
authors.forename: Kazuhisa
authors.initials: K
authors.lastname: Takahashi
mesh_terms: D000818:Animals; D001253:Astrocytes / Q000378:metabolism*; D020516:Brachial Plexus Neuropathies / Q000378:metabolism* / Q000628:therapy; D004195:Disease Models, Animal; D006930:Hyperalgesia / Q000378:metabolism* / Q000628:therapy; D007150:Immunohistochemistry; D008297:Male; D017628:Microglia / Q000378:metabolism*; D010147:Pain Measurement; D020671:Posterior Horn Cells; D051381:Rats; D017208:Rats, Wistar