Article Figures & Data
Figures
- Fig. 1.
Synaptophysin immunoreactivity in the dentate gyrus of ECL wild-type and ApoE-KO mice. C57BL/6J mice (A–C) and apoE-KO mice (D–F) showed different responses to estradiol after ECL. Two weeks after surgery, sham-OVX mice (A, WT; D, apoE-KO) showed less immunoreactivity in the middle molecular layer than in the inner or outer layer of the dentate gyrus. In wild-type C57BL/6J mice, OVX causes a decrease in both the relative thickness and OD of the inner layer (B), whereas estradiol replacement brought inner layer thickness and OD back to sham-OVX levels (C). In apoE-KO mice, OVX (E) and estradiol replacement (F) made no significant changes in inner molecular layer thickness or OD. Width of the outer molecular layer was also increased in the WT E2-replaced mice (C). In apoE-KO mice, outer molecular layer width was unaffected by estrogen treatment (D–F).H, Hilus; G, granular layer;O, outer; M, middle; I, inner molecular layer.
- Fig. 2.
Markers for sprouting in response to ECL show E2-dependent effects in wild-type but not ApoE-KO mice.A, The absolute width and OD of SYN immunoreactivity in the inner molecular layer were measured with an image-processing analysis system, and integrated density (thickness × optical density) was calculated. The y-axis gives integrated density as a percent of that for the WT, ovary-bearing (control) mice. There was a decrease in both thickness (15%; p < 0.05) and OD (35%; p < 0.05) of the inner layer of WT ovariectomized mice. E2 replacement returned inner layer width, OD, and integrated density to control levels. ApoE-KO mice did not show any significant changes in response to E2. Ovary-bearing apoE-KO mice showed a reduced integrated density (15%; NS) when compared with ovary-bearing controls. *Significantly different from control; p < 0.05. B, The OD of the outer molecular layer reached the threshold of image analysis software; however, the width of the outer layer was measured. They-axis gives the width of the outer molecular layer, expressed as a percent of the total molecular layer width. Although OVX did not cause a significant decrease in outer layer width in WT mice, E2-replaced mice showed a significant increase in outer layer width. In contrast, no E2 effect on outer molecular layer width was detected in aopE-KO mice. *Significantly different from inner layer width; p < 0.05.
- Fig. 3.
ApoJ mRNA levels show E2-dependent effects in wild-type but not ApoE-KO mice. A, At the lesion site (entorhinal cortex), apoJ mRNA level shows a nonsignificant decrease in response to OVX and a 1.7-fold increase with E2replacement. No significant changes were observed in apoE-KO mice. They-axis gives in situ grain density as a percent of WT, ovary-bearing (control) mice. B, In the deafferented dentate gyrus (ipsilateral to lesion), apoJ mRNA levels did not change in WT mice, whereas apoE-KO mice showed increased apoJ mRNA levels in response to ovariectomy. E2 replacement did not have an effect. Levels are given as a percent of contralateral values. The y-axis gives in situ grain density expressed as a percent of that in the contralateral (unlesioned) dentate gyrus of the same brain. C, In the unlesioned hippocampus (contralateral to lesion) of sham-ovariectomized mice, apoE-KO mice showed a nonsignificant increase in apoJ mRNA, suggesting a possible compensatory increase. This trend did not extend to the apoJ responses to E2 or lesion. They-axis gives the in situ grain density in the unlesioned dentate gyrus, expressed as a percent of that in WT mice. *Significantly different from sham-OVX mice;p < 0.05.
Tables
Treatment Wild-type C57B1/6J ApoE-KO Weight (mg) SE Weight (mg) SE Control 72 9 65 6 OVX 20* 2 18* 2 OVX + E2 183* 16 165** 15 OVX caused a threefold decrease, and E2 replacement caused a 2.5-fold increase in uterine weight in both WT and apoE-KO mice. There were no significant strain or strain × treatment interaction effects.
*p < 0.0001.
**p < 0.01.
