Glucose infusion suppresses neuronal damage following kainate-induced status epilepticus. (A) Low-magnification photomicrographs of cresyl violet (A,D,G) and NeuN-immunofluorescent (B,E,F) stained horizontal sections of the hippocampus illustrating surviving cells throughout the hippocampus 7 days following systemic kainate administration to FVB mice. High-magnification NeuN-immunofluorescent stained horizontal sections of area CA3 (C,F,I) among the three groups. Neuron loss following status epilepticus was profoundly reduced when exogenous glucose was administered for 3 consecutive days following seizure induction. Note the significant amount of cell loss in representative sections from KA-treated mice in the dentate hilus, area CA3 and area CA1, depicted as an absence of cresyl violet stain (D) or NeuN-immunofluorescence (E). Cell loss was not observed after post-seizure glucose infusion (G,H,I). 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 KA administration to FVB mice. Viable surviving neurons were estimated by cresyl violet staining. Bars denote the percentage of surviving neurons (as compared with saline-injected sham control FVB 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; a: F=9.68, P=0.003; b: F=42.87, P<0.001; c: F=23.76, P<0.001).
Schauwecker BMC Neuroscience 2012 13:94 doi:10.1186/1471-2202-13-94