Figure 11.

Effect of estrogens, 17β-estradiol and Δ 8,17β-estradiol, on glutamate-induced cleavage of α-fodrin in HT22 cells and primary cortical cells. A: HT22 cells were treated with 7 mM glutamate in the presence or absence of 1 μM and 10 μM 17β-estradiol or Δ8,17β-estradiol for 8 hrs. B: primary cortical cells isolated from 18 day old fetal rat brains were cultured for 7–8 days and treated with 1 mM glutamate in the presence or absence of 1 μM and 10 μM 17β-estradiol or Δ8,17β-estradiol for 6 hrs. A, B: (I): representative Western blots showing calpain and caspase-3-mediated proteolysis of α-fodrin and inhibition by estrogens. A, B: (II): semi-quantitative analysis of calpain and caspase-3-mediated proteolysis of α-fodrin. Accumulation of breakdown products was assessed by Western blot analysis as described under Figure 9. Actin was used as a loading control. The bar depict densitometric analysis of Western blots from at least three experiments (± SEM) *P < 0.05 compared to control; P < 0.05 compared to glutamate alone.

Zhang and Bhavnani BMC Neuroscience 2006 7:49   doi:10.1186/1471-2202-7-49
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