Role of Inflammatory Mediators in the Pathogenesis of Epilepsy

Figure 2

mPGES-1-KO mice show a less severe aggravation of epileptic seizures. (a) Development of epileptic convulsive seizures following consecutive treatments with PTZ. Two-month-old female C57/BL6 background mice of WT or mPGES-1-KO mice were injected intraperitoneally with a subconvulsive dose (35 mg/kg) of PTZ every other day. After each PTZ injection, the convulsive behaviors were observed for 30 min and the resultant seizures were classified and scored as follows: 0: normal behavior; 1: immobilization; 2: facial, forelimb, or hindlimb myoclonus; 3: continuous whole body myoclonus; 4: rearing, tonic seizure; 5: tonic-chronic seizure; and 6: death [12]. mPGES-1-KO mice showed significant reduction in seizure score compared with that in WT mice (*: , repeated-measured ANOVA). (b) Representative images of the CA3 region of hippocampal sections from WT and mPGES-1-KO mice after PTZ-induced chemical kindling. Mice were fixed with 4% paraformaldehyde. Serial sections (30 μm) were generated, and immunostaining was performed with a rabbit anti-GFAP antibody (DAKO). Gliosis was observed only in the sections from wild type mice. Scale  μm. (c) Quantification of gliosis development: squares were randomly overlaid on the CA3 region of hippocampal slices and the percentage of pixels that had a higher intensity of GFAP signal than the threshold was compared. The GFAP-positive area was significantly increased after kindling in WT mice, whereas no increase was observed in mPGES-1-KO mice (, two-way ANOVA followed by Tukey’s test). Six squares were taken from one brain slice. Four slices were examined under each condition.