Figure 3.

Number of GFP-positive hilar neurons, length of GFP-positive axon in the dentate gyrus, and related parameters of control mice and mice that experienced pilocarpine-induced status epilepticus and then were treated daily for two months with vehicle or 3 mg/kg rapamycin. A Vehicle- and rapamycin-treated mice had fewer GFP-positive hilar neurons compared to controls (*p < 0.001, ANOVA with Student-Newman-Keuls Method). There was no significant difference between vehicle- and rapamycin-treated mice. Error bars indicate s.e.m. Each group consisted of 6 mice. B Vehicle-treated mice had more GFP-positive axon per dentate gyrus compared to control and rapamycin-treated mice (*p < 0.001). There was no significant difference between control and rapamycin-treated mice. C Average GFP-positive axon density was slightly elevated in vehicle-treated mice but not significantly different among experimental groups (p = 0.068). D Average number of GFP-positive axon crossings of the granule cell layer was similar among experimental groups. E GFP-positive axon length correlated with number of granule cells per dentate gyrus (p = 0.006, R² = 0.385). F GFP-positive axon length correlated with volume of the dentate gyrus (p < 0.001, R² = 0.871).