title: Role of TRPM2 cation channels in dorsal root ganglion of rats after experimental spinal cord injury.
abstract: BACKGROUND
  We sought to determine the contribution of oxidative stress-dependent activation of TRPM2 and L-type voltage-gated Ca(2+) channels (VGCC) in dorsal root ganglion (DRG) neurons of rats after spinal cord injury (SCI).
  
  
  METHODS
  The rats were divided into 4 groups: control; sham control; SCI; and SCI+nimodipine groups. The neurons of the SCI groups were also incubated with non-specific TRPM2 channel blockers, 2-aminoethoxydiphenylborate (2-APB) and N-(p-amylcinnamoyl)anthranilic acid (ACA), before H2 O2 stimulation.
  
  
  RESULTS
  The [Ca(2+) ]i concentrations were higher in the SCI group than in the control groups, although their concentrations were decreased by nimodipine and 2-APB. The H2 O2 -induced TRPM2 current densities in patch-clamp experiments were decreased by ACA and 2-APB incubation. In the nimodipine group, the TRPM2 channels of neurons were not activated by H2 O2 or cumene hydroperoxide.
  
  
  CONCLUSIONS
  Increased Ca(2+) influx and currents in DRG neurons after spinal injury indicated TRPM2 and voltage-gated Ca(2+) channel activation.
authors.affiliation: Department of Biophysics, Medical Faculty, Suleyman Demirel University, Isparta, Turkey; Neuroscience Research Center, Suleyman Demirel University, TR-32260, Isparta, Turkey.
authors.forename: Mustafa
authors.initials: M
authors.lastname: Naziroğlu
authors.forename: Abdülhadi Cihangir
authors.initials: AC
authors.lastname: Uğuz
authors.forename: Özgür
authors.initials: Ö
authors.lastname: Ismailoğlu
authors.forename: Bilal
authors.initials: B
authors.lastname: Çiğ
authors.forename: Cemil
authors.initials: C
authors.lastname: Özgül
authors.forename: Muhammed
authors.initials: M
authors.lastname: Borcak
mesh_terms: D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000818:Animals; D001896:Boron Compounds / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism; D020746:Calcium Channels, L-Type / Q000378:metabolism; D002934:Cinnamates / Q000494:pharmacology; D004195:Disease Models, Animal; D005727:Ganglia, Spinal / Q000378:metabolism* / Q000473:pathology; D006861:Hydrogen Peroxide / Q000494:pharmacology; D008297:Male; D009474:Neurons / Q000187:drug effects / Q000502:physiology; D016877:Oxidants / Q000494:pharmacology; D018408:Patch-Clamp Techniques; D051381:Rats; D017208:Rats, Wistar; D013119:Spinal Cord Injuries / Q000473:pathology*; D018709:Statistics, Nonparametric; D050053:TRPM Cation Channels / Q000037:antagonists & inhibitors / Q000378:metabolism*; D062367:ortho-Aminobenzoates / Q000494:pharmacology
chemical_list: D001896:Boron Compounds; D020746:Calcium Channels, L-Type; D002934:Cinnamates; D016877:Oxidants; D050053:TRPM Cation Channels; C557080:Trpm2 protein, rat; D062367:ortho-Aminobenzoates; C085901:4-amylcinnamoylanthranilic acid; D006861:Hydrogen Peroxide; C109986:2-aminoethoxydiphenyl borate; D002118:Calcium
keywords: Ca2+ signaling; TRPM2 cation channels; nimodipine; oxidative stress; peripheral pain; spinal injury