Figure 3

Glucose infusion suppresses neuronal damage following kainate-induced status epilepticus damage. (A) Blood glucose concentration was decreased significantly 3 hours after insulin injection and after insulin + kainate injections. Data represent the mean ± S.E.M. of at least 5 mice per condition. Asterisk indicates significant difference compared with any other group (ANOVA with post hoc Student Newman Keuls; F=16.57, P<0.001). (B) Quantitative analysis of neuronal density in hippocampal subfields following insulin injection + KA 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 (ANOVA with post hoc Student Newman Keuls; F=99.70, P<0.001). (C) Insulin-induced hypoglycemia dramatically increased the extent of hippocampal cell death in B6 mice. Low-power photomicrographs of cresyl violet (A,D,G) and NeuN-stained (B,E,H) horizontal sections of the hippocampus showing differential cell loss 7 days after kainate-induced SE in a normoglycemic (NS + KA) and hypoglycemic (insulin + KA) mouse. Note that extensive kainate-induced cell loss, as evidenced by loss of cresyl violet staining (G) and NeuN immunostaining (H), is only observed in the dentate hilus, areas CA3 and CA1 following insulin pre-treatment in excitotoxin cell death resistant (B6) mice. 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.