Figure 5

Diabetic-induced hyperglycemia aggravates status epilepticus-induced hippocampal damage. (A) Low-power photomicrographs of cresyl violet (A,D,G) and NeuN-immunofluorescent-stained (B,E,H) horizontal sections of the hippocampus illustrating surviving cells throughout the hippocampus 7 days following systemic kainate administration to vehicle-treated, and STZ-treated mice that underwent KA-induced SE. STZ-induced hyperglycemia dramatically increased the extent of hippocampal cell death in excitotoxin cell death resistant B6 mice. Note the significant amount of cell damage in representative sections from STZ + KA treated mice as evidenced by a loss of cresyl violet staining (G) and NeuN-immunofluorescence (H) and complete absence of any seizure-associated cell loss in KA treated mice (D,E). CA1 and CA3 denote the hippocampal subfields; H, dentate hilus. Scale bar = 750 μm (A,C); 100 μm (B,D). High-magnification photomicrographs represent details of the boxed area of CA3 shown in B. (B) Quantitative analysis of neuronal density in hippocampal subfields seven days following STZ + KA administration to B6 mice. Viable surviving neurons were estimated by cresyl violet staining. Bars denote the percentage of surviving neurons (as compared with saline-injected sham control B6 mice). Data represent the mean ± S.E.M. of at least 5 mice per condition. Asterisks indicate significant difference compared with KA alone or Sham control of P<0.05. (ANOVA with post hoc Student Newman Keuls; F=195.54, P<0.001).