title: [Effect of carbenoxolone on expression of Fos, NMDAR2 and GFAP in the hippocampus of pentylenetetrazo-kindled epileptic rats].
abstract: OBJECTIVE
  Gap junctions, the clusters of intercellular channels, play an important role in synchronizing electrical activity. This study investigated the effect of gap junction blocker carbenoxolone (CBX) on epileptic activity in pentylenetetrazo (PTZ)-kindled rats.
  
  
  METHODS
  Thirty adult male SD rats were randomly divided into three groups: control, PTZ-kindled and CBX-treated groups (n=10 each). The rats from the PTZ-kindled and the CBX-treated groups were intraperitoneally injected with PTZ (35 mg/kg x d) to induce epilepsy. After epilepsy kindling, they were intraperitoneally injected for 3 days with CBX (10 mg/kg) (CBX-treated group) or with normal saline (PTZ-kindled group). The control group received intraperitoneal injections of normal saline. Anti-GFAP, anti-Fos, and anti-NMDARZ immunohistochemical ABC methods were used to detect the expression of GFAP-Li, Fos-Li and NMDAR2-Li in the hippocampus respectively.
  
  
  RESULTS
  Spontaneous seizures occurred in PTZ-kindled epileptic rats. CBX administration reduced spontaneous seizures. The NMDAR2-Li and Fos-Li neurons as well as GFAP-Li astrocytes in hippocampi increased in PTZ-kindled epileptic rats compared with controls. The numbers of Fos-Li (93.75 +/-7.94 vs 165.25 +/-15.87, P < 0.05) and NMDAR2-Li neurons (61.47 +/-3.62 vs 148.72 +/-14.53, P < 0.01) in the CBX-treated group were significantly less than in the PTZ-kindled group. There were no significant differences in the GFAP-Li expression between the CBX-treated and the PTZ-kindled groups.
  
  
  CONCLUSIONS
  CBX may inhibit spontaneous seizures and decrease the numbers of Fos-Li and NMDARZ-Li neurons, thus providing anti-epileptic effects.
authors.affiliation: Department of Pediatrics, Tangdu Hospital, Fourth Military Medical Unversity, Xi'an 710038, China.
authors.forename: Li
authors.initials: L
authors.lastname: Lan
authors.forename: Bao-Xi
authors.initials: BX
authors.lastname: Wang
authors.forename: Xin
authors.initials: X
authors.lastname: Zhao
authors.forename: Li
authors.initials: L
authors.lastname: Duan
authors.forename: Rong
authors.initials: R
authors.lastname: Cao
authors.forename: Yu
authors.initials: Y
authors.lastname: Liu
authors.forename: Zhi-Ren
authors.initials: ZR
authors.lastname: Rao
mesh_terms: D000818:Animals; D002229:Carbenoxolone / Q000494:pharmacology*; D004827:Epilepsy / Q000188:drug therapy* / Q000378:metabolism; D017629:Gap Junctions / Q000187:drug effects*; D005904:Glial Fibrillary Acidic Protein / Q000032:analysis*; D006624:Hippocampus / Q000187:drug effects* / Q000378:metabolism; D007150:Immunohistochemistry; D007696:Kindling, Neurologic / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D010433:Pentylenetetrazole; D016760:Proto-Oncogene Proteins c-fos / Q000032:analysis*; D051381:Rats; D017207:Rats, Sprague-Dawley; D016194:Receptors, N-Methyl-D-Aspartate / Q000032:analysis*
chemical_list: D002229:Carbenoxolone; D005904:Glial Fibrillary Acidic Protein; D010433:Pentylenetetrazole; D016760:Proto-Oncogene Proteins c-fos; D016194:Receptors, N-Methyl-D-Aspartate; C121001:NR2B NMDA receptor