title: Effect of lumbar nerve root compression on primary sensory neurons and their central branches: changes in the nociceptive neuropeptides substance P and somatostatin.
abstract: METHODS
  This study examined the effect of lumbar nerve root compression on nociceptive neuropeptides in the axonal flow using an in vivo model.
  
  
  OBJECTIVE
  The aim was to investigate changes in axonal flow after nerve root compression by using immunohistochemical techniques to detect substance P (SP) and somatostatin (SOM), which is thought to be involved in temperature and pain sensation.
  
  
  BACKGROUND
  Disturbance of intraradicular blood flow and nerve fiber deformation caused by mechanical compression are thought to be involved in the pathophysiology of diseases characterized by radicular symptoms, such as lumbar disc herniation and lumbar canal stenosis. However, little research has been conducted into the changes of axonal flow associated with nerve root compression.
  
  
  METHODS
  In dogs, the lumbar nerve roots were compressed using four types of clips with different pressures. Changes of SP and SOM levels in the spinal dorsal horn, dorsal root, and dorsal root ganglions were examined immunohistochemically after compression for 24 hours or 1 week.
  
  
  RESULTS
  After compression for 24 hours, axonal flow in the dorsal root was impaired, accumulation of SP and SOM was observed distal to the site of compression, and there was a decrease in the number of dorsal root ganglion cells showing positively for these neurotransmitters. Compression for 1 week resulted in a decrease in the number of SP- and SOM-positive fibers in the spinal dorsal horn.
  
  
  CONCLUSIONS
  Change of axonal flow resulting from direct nerve compression could affect the metabolism of neurotransmitters that flow inside the axons and may be a primary cause of the decline in nerve function.
authors.affiliation: Department of Orthopaedics and Rehabilitation Medicine, Fukui University School of Medicine, Fukui, Japan. kshigeru@fmsrsa.fukui-med.ac.jp
authors.forename: Shigeru
authors.initials: S
authors.lastname: Kobayashi
authors.forename: Yasuo
authors.initials: Y
authors.lastname: Kokubo
authors.forename: Kenzo
authors.initials: K
authors.lastname: Uchida
authors.forename: Takafumi
authors.initials: T
authors.lastname: Yayama
authors.forename: Kenichi
authors.initials: K
authors.lastname: Takeno
authors.forename: Kouhei
authors.initials: K
authors.lastname: Negoro
authors.forename: Hideaki
authors.initials: H
authors.lastname: Nakajima
authors.forename: Hisatoshi
authors.initials: H
authors.lastname: Baba
authors.forename: Hidezo
authors.initials: H
authors.lastname: Yoshizawa
mesh_terms: D000818:Animals; D001370:Axonal Transport; D015415:Biomarkers / Q000378:metabolism; D002452:Cell Count; D004195:Disease Models, Animal; D004285:Dogs; D005727:Ganglia, Spinal / Q000293:injuries / Q000473:pathology / Q000503:physiopathology; D007091:Image Processing, Computer-Assisted; D007124:Immunoenzyme Techniques; D008159:Lumbar Vertebrae; D009408:Nerve Compression Syndromes / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D020671:Posterior Horn Cells / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D011843:Radiculopathy / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D013004:Somatostatin / Q000378:metabolism*; D013373:Substance P / Q000378:metabolism*
chemical_list: D015415:Biomarkers; D013373:Substance P; D013004:Somatostatin