title: Spinal neuropeptide responses in persistent and transient pain following cervical nerve root injury.
abstract: METHODS
  Behavioral and immunohistochemical analysis in rat models of persistent and transient allodynia.
  
  
  OBJECTIVE
  To examine separate cervical nerve root injuries (compression, transection) for producing behavioral hypersensitivity and investigate spinal neuropeptides to understand relationships to pain symptoms.
  
  
  BACKGROUND
  Mechanical cervical nerve root injury can be a source of neck pain. Painful lumbar radiculopathy models show that different nerve root ligation intensities produce differential allodynia responses. Spinal neuropeptides can mediate pain responses. Yet, little is known about their contributions to pain in the cervical spine.
  
  
  METHODS
  Rats underwent separate procedures on the right C7 nerve roots: transection (n = 12), 10-gf compression for 15 minutes (n = 11), or sham (n = 5). Ipsilateral forepaw mechanical allodynia was measured after surgery for 7 days. C7 spinal cord tissue was analyzed by immunohistochemistry for substance P and calcitonin gene-related peptide (CGRP) expression on days 1 and 7 for each injury; densitometry quantified immunoreactivity in lamina I of the ipsilateral dorsal horn.
  
  
  RESULTS
  Both injuries immediately produced significant increases in allodynia. Sensitivity was sustained following root compression, and at day 7, was not different from day 1. By day 7 after transection, allodynia had returned to baseline and sham levels, significantly decreasing from day 1 (P = 0.0012). Spinal substance P and CGRP were increased over normal at day 1 for both injuries and decreased with time for CGRP after transection, which paralleled behaviors. For individual rats, substance P was significantly (P < 0.001) correlated with CGRP expression for both injuries.
  
  
  CONCLUSIONS
  Compression and transection of the cervical nerve root produce different forepaw allodynia responses, with persistent and transient sensitivity, respectively. Spinal neuropeptide expression in these models parallels this sensitivity, suggesting their potential role in pain symptoms.
authors.affiliation: Department of Bioengineering, University of Pennsylvania, Philadelphia, Pennsylvania 19104-6392, USA.
authors.forename: Sarah M
authors.initials: SM
authors.lastname: Rothman
authors.forename: Rob A
authors.initials: RA
authors.lastname: Kreider
authors.forename: Beth A
authors.initials: BA
authors.lastname: Winkelstein
mesh_terms: D000208:Acute Disease; D000818:Animals; D015740:Calcitonin Gene-Related Peptide / Q000378:metabolism*; D002574:Cervical Vertebrae; D002908:Chronic Disease; D006930:Hyperalgesia / Q000378:metabolism; D007150:Immunohistochemistry; D008297:Male; D019547:Neck Pain / Q000378:metabolism; D009437:Neuralgia / Q000378:metabolism*; D011843:Radiculopathy / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013116:Spinal Cord / Q000378:metabolism*; D013126:Spinal Nerve Roots / Q000293:injuries*; D013373:Substance P / Q000378:metabolism*
chemical_list: D013373:Substance P; D015740:Calcitonin Gene-Related Peptide