| apoE2 | apoE3 | apoE4 |
---|
 | saline | LPS | Saline | LPS | saline | LPS |
Sholl r (μm)
|
microns
|
% of saline
|
microns
|
% of saline
|
microns
|
% of saline
|
0–50 | 523 ± 38 | 52.9 ± 5.1 | 497 ± 48 | 44.7 ± 3.3 | 542 ± 36 | 44.6 ± 4.7 |
51–100 | 497 ± 36 | 40.1 ± 4.9 | 456 ± 47 | 36.8 ± 10.0 | 513 ± 39 | 36.9 ± 7.2 |
101–150 | 98 ± 13 | 42.2 ± 10.4 | 80 ± 10 | 30.0 ± 10.1 |
58 ± 8^
| 33.1 ± 9.8 |
- Total dendrite length for each Sholl compartment for mouse pyramidal neurons within hippocampal sector CA1 was determined by Golgi staining followed by analysis with Neurolucida. Data are from the three lines of TR APOE mice with four mice from each genotype examined at this time point. For PBS-treated mice (n = 6 neurons per mouse in each group for a total of 12 neurons per genotype and exposure), two-way ANOVA had P < 0.0001 for Sholl compartment but P > 0.05 for TR APOE; however, one-way ANOVA in the distal Sholl compartment of the three genotypes had P < 0.05 and Bonferroni-corrected repeated pair comparisons had ^P < 0.05 for TR APOE2 vs. TR APOE4 but no other paired comparisons. For ICV LPS-exposed mice, two-way ANOVA was not significant for TR APOE or Sholl compartment at 24 hr post ICV LPS (n = 6 neurons per mouse in each group for a total of 12 neurons per genotype and exposure), nor was one-way ANOVA across any of the Sholl compartments. These values encompass our previous results with ICV LPS in C57Bl/6 mice [3, 17, 18]