title: Systemic antiinflammatory corticosteroid reduces mechanical pain behavior, sympathetic sprouting, and elevation of proinflammatory cytokines in a rat model of neuropathic pain.
abstract: BACKGROUND
  Chronic pain models are commonly defined as either nerve-injury or inflammation models, but recent work suggests inflammatory processes are important in nerve injury-induced pain.
  
  
  METHODS
  In the rat spinal nerve ligation model, the authors examined effects of systemic corticosteroid triamcinolone acetonide (TA) on the cytokine protein profile and sympathetic sprouting in the axotomized sensory ganglia, excitability of sensory neurons, and mechanical sensitivity.
  
  
  RESULTS
  By postoperative day 3, marked increases (5- to 16-fold) in monocyte chemoattractant protein-1, growth-related oncogene (GRO/KC or CXCL1), and interleukin (IL)-6 were observed, whereas IL-4 and IL-2 levels fell more than fourfold. The increased cytokines and number of sympathetic basket formations in the sensory ganglia were reduced toward normal values by TA given starting at the time of injury. Interleukin-4 and IL-2 levels were not restored by TA. Systemic TA also reduced the firing rate and incidence of bursting activity, but not the overall incidence of spontaneous activity, in large- and medium-sized neurons. Mechanical hypersensitivity on postoperative day 3 was reduced by TA, and some effect could still be observed 4 days after cessation of TA. However, starting TA at day 7 was ineffective.
  
  
  CONCLUSIONS
  Several components of the spinal nerve injury model are responsive to corticosteroid, suggesting inflammatory processes are important in the development of neuropathic pain. The observation that TA was effective when given starting at the time of injury suggests that steroid treatment might alter the development of chronic pain after surgical procedures that involve nerve injury, such as amputation or hernia repair.
authors.affiliation: Pain Research Center, Department of Anesthesiology, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267-0531, USA.
authors.forename: Huiqing
authors.initials: H
authors.lastname: Li
authors.forename: Wenrui
authors.initials: W
authors.lastname: Xie
authors.forename: Judith A
authors.initials: JA
authors.lastname: Strong
authors.forename: Jun-Ming
authors.initials: JM
authors.lastname: Zhang
mesh_terms: D000305:Adrenal Cortex Hormones / Q000627:therapeutic use*; D000320:Adrenergic Fibers / Q000187:drug effects*; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D001522:Behavior, Animal / Q000187:drug effects*; D016207:Cytokines / Q000187:drug effects*; D004195:Disease Models, Animal; D008297:Male; D009437:Neuralgia / Q000188:drug therapy*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013127:Spinal Nerves / Q000187:drug effects* / Q000503:physiopathology; D013997:Time Factors; D014222:Triamcinolone Acetonide / Q000627:therapeutic use*
chemical_list: D000305:Adrenal Cortex Hormones; D000893:Anti-Inflammatory Agents; D016207:Cytokines; D014222:Triamcinolone Acetonide