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. 2003 Aug 18;100(18):10506–10511. doi: 10.1073/pnas.1334098100

Fig. 1.

Fig. 1.

E2 and P4, but not MPA, attenuate the excitotoxic glutamate-induced rise in [Ca2+]i. Hippocampal neurons pretreated with E2 (10 ng/ml), P4 (PRG), or both exhibited a significantly lower response to glutamate (200 μM) than control neurons. MPA had no effect on glutamate-induced Ca2+ signaling, but blocked the estrogen-mediated attenuation. (A) Representative tracings of the average [Ca2+]i from 10 neurons over time in response to glutamate in the presence or absence of P4 and/or E2.(B) Quantitative changes in [Ca2+]i in response to glutamate in the presence or absence of P4 and/or E2.(C) Representative tracings of the average [Ca2+]i from 10 neurons over time in response to glutamate in the presence or absence of MPA and/or E2. (D) Quantitative changes in [Ca2+]i in response to glutamate in the presence or absence of MPA and/or E2. *, P < 0.05 vs. control neurons; **, P < 0.01 vs. control neurons; ++, P < 0.01 vs. E2-treated neurons; n = 4 independent experiments with ≥10 neurons per experiment.