title: Trauma-induced reactive gliosis is reduced after treatment with octanol and carbenoxolone.
abstract: BACKGROUND
  Reactive gliosis and scar formation after brain injury can inhibit the recovery process. As many glial cells utilize gap junctions for intercellular signaling, this study investigated whether two commonly used gap junction blockers, octanol and carbenoxolone, could attenuate reactive gliosis following a minor traumatic brain injury.
  
  
  METHODS
  Octanol (710 mg/kg) or carbenoxolone (90 mg/kg) was administered 30 minutes before or after a needle track injury in adult male Sprague-Dawley rats. To mark dividing cells, animals were injected with bromodeoxyuridine (BrdU; 150 mg/kg) intraperitoneally two times per day, 8 hours apart and killed 2 days later. Immunohistochemistry for BrdU and markers for reactive glial cells [glial fibrillary acidic protein (GFAP), ED1, and NG2] were investigated using immunohistochemistry and western blot techniques.
  
  
  RESULTS
  Two days after injury, increased cellular proliferation, activated astrocytes and microglia, and upregulation of NG2 expression were observed surrounding the injury site. Octanol and carbenoxolone administrated prior to injury significantly decreased cell proliferation by 60 and 70% respectively. The distance of GFAP immunoreactive astrocytes from the wound margin was decreased by 32 and 18% when octanol was administrated prior to or post injury respectively. Treatment with octanol also decreased the number of reactive microglia by 55% and, when administrated prior to injury, octanol reduced the distance of NG2 expression from the wound by 48%.
  
  
  CONCLUSIONS
  The present study demonstrates that two important components of reactive gliosis, cellular activation and proliferation, can be attenuated by octanol and carbenoxolone.
authors.affiliation: Center for Brain Repair and Rehabilitation, Institute of Neuroscience and Physiology, University of Gothenburg, Medicinaregatan 11, Box 432, SE-40530 Gothenburg, Sweden.
authors.forename: Heléne C
authors.initials: HC
authors.lastname: Andersson
authors.forename: Michelle F
authors.initials: MF
authors.lastname: Anderson
authors.forename: Michelle J
authors.initials: MJ
authors.lastname: Porritt
authors.forename: Christina
authors.initials: C
authors.lastname: Nodin
authors.forename: Fredrik
authors.initials: F
authors.lastname: Blomstrand
authors.forename: Michael
authors.initials: M
authors.lastname: Nilsson
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D001930:Brain Injuries / Q000150:complications / Q000188:drug therapy* / Q000473:pathology; D002229:Carbenoxolone / Q000627:therapeutic use*; D002478:Cells, Cultured; D005911:Gliosis / Q000188:drug therapy* / Q000209:etiology / Q000473:pathology; D008297:Male; D000442:Octanols / Q000627:therapeutic use*; D051381:Rats; D017207:Rats, Sprague-Dawley; D016896:Treatment Outcome
chemical_list: D000442:Octanols; D002229:Carbenoxolone