title: Sympathectomy and Sympathetic Blockade Reduce Pain Behavior Via Alpha-2 Adrenoceptor of the Dorsal Root Ganglion Neurons in a Lumbar Radiculopathy Model.
abstract: METHODS
  Animal experimental study with intervention.
  
  
  OBJECTIVE
  We investigated whether sympathectomy and pharmacological sympathetic blockade reduced pain behavior and reversed adrenoceptor mRNA expression of the dorsal root ganglion (DRG) in a lumbar radiculopathy model.
  
  
  BACKGROUND
  The abnormal sympathetic-somatosensory interaction may underlie some forms of neuropathic pain. There are several reports that sympathectomy and pharmacological sympathetic blockades are often effective to treat neuropathic pain. However, its pathophysiological mechanisms remain obscure.
  
  
  METHODS
  We used 91 male Sprague-Dawley rats. Just after root constriction (RC), the rats underwent sympathectomy or received 3 local injections of subtype-specific α-adrenergic receptor antagonists around the DRG. We evaluated the analgesic effects of sympathectomy and sympathetic blockade using behaviors indicative mechanical allodynia and thermal hyperalgesia. We estimated the mRNA expression levels of the DRG adrenoceptor subtypes using real time reverse transcription polymerase chain reaction.
  
  
  RESULTS
  Sympathectomy and α2-antagonist significantly reduced the mechanical allodynia and thermal hyperalgesia after RC. Real time reverse transcription polymerase chain reaction analysis indicated that sympathectomy possibly reversed α2A- and α2B-adrenoceptors mRNA overexpression in the DRG after RC.
  
  
  CONCLUSIONS
  We considered that pain behaviors of neuropathic pain are due, at least in part, to enhanced sympathetic noradrenergic transmission within the DRG. Suppression of sympathetic activity by reducing adrenergic release, α2-adrenoceptor stimulation, and/or α2-adrenoceptor upregulation in the DRG may relieve neuropathic pain.
  
  
  METHODS
  3.
authors.affiliation: *Departments of Orthopaedic Surgery†Cellular Physiology and Signal Transduction, Sapporo Medical University School of Medicine, Hokkaido, Japan.
authors.forename: Izaya
authors.initials: I
authors.lastname: Ogon
authors.forename: Tsuneo
authors.initials: T
authors.lastname: Takebayashi
authors.forename: Takehito
authors.initials: T
authors.lastname: Iwase
authors.forename: Makoto
authors.initials: M
authors.lastname: Emori
authors.forename: Katsumasa
authors.initials: K
authors.lastname: Tanimoto
authors.forename: Tsuyoshi
authors.initials: T
authors.lastname: Miyakawa
authors.forename: Yoshinori
authors.initials: Y
authors.lastname: Terashima
authors.forename: Takeshi
authors.initials: T
authors.lastname: Kobayashi
authors.forename: Noritsugu
authors.initials: N
authors.lastname: Tohse
authors.forename: Toshihiko
authors.initials: T
authors.lastname: Yamashita
mesh_terms: D000818:Animals; D001522:Behavior, Animal; D004195:Disease Models, Animal; D005727:Ganglia, Spinal / Q000503:physiopathology / Q000601:surgery*; D006930:Hyperalgesia; D008297:Male; D010146:Pain / Q000503:physiopathology*; D011843:Radiculopathy / Q000601:surgery*; D051381:Rats; D017207:Rats, Sprague-Dawley; D018341:Receptors, Adrenergic, alpha-2 / Q000378:metabolism*; D013562:Sympathectomy / Q000379:methods*
chemical_list: D018341:Receptors, Adrenergic, alpha-2