FIGURE 3. E2 Ameliorates Aβ-induced Inhibition of GluR1 Phosphorylation and Decreased GluR1 Membrane Insertion.

A) E2 ameliorates Aβ-induced inhibition of GluR1 phosphorylation in primary cortical neurons. Primary cortical neurons (E18) were grown 15 DIV and were pretreated with soluble Aβ_1–42 oligomers (0.5 µM) for 24 hrs. Neurons were then treated with or without E2 (10 nM) for 1 hr in the presence or absence of KN-93. Aβ treatment decreased GluR1 phosphorylation (63 ± 10%), while E2 ameliorated Aβ’s effect (317 ± 38%). E2-induced phosphorylation was inhibited by KN-93 (218 ± 55%). B) GluR1 insertion into the membrane of primary cortical neurons. Primary cortical neurons (E18) were grown 15 DIV and were pretreated with soluble Aβ_1–42 oligomers (0.5 µM) for 24 hrs. E2 (10 nM) treatment for 1 hr increased surface expression of pGluR1 (serine 831) and Aβ treatment inhibited this surface expression (338 ± 46% and 49 ± 10%, respectively). The surface expression of pGluR1 (serine 831) was normalized with surface expression of GABA receptor. E2 treatment ameliorated Aβ-induced inhibition of GluR1 insertion into the membrane of cortical neurons (270 ± 17%). Data are mean ± SD. **, p<0.01, ***, p<0.001, versus control or groups connected by bars as determined by one-way ANOVA followed by Newman-Keuls Multiple Comparison Test, n=3 (3 independent experiments).