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. 2005 May 18;25(20):5066–5078. doi: 10.1523/JNEUROSCI.1427-05.2005

Figure 6.

Figure 6.

Estradiol-mediated CREB phosphorylation occurs via activation of mGluR1a signaling, independent of glutamate release. A, The mGluR1a antagonist/inverse agonist LY367385 (100 μm) eliminated estradiol-mediated CREB phosphorylation, without affecting estradiol inhibition of depolarization-induced CREB phosphorylation (F = 45.18; **p < 0.01 vs 17βE). B, The mGluR1/5 agonist DHPG (50 μm) in the presence of the mGluR5 antagonist MPEP (5 μm) increased CREB phosphorylation in cultures derived from female animals similar to estradiol and occluded the steroid effect (F = 49.98; **p < 0.01). C, DHPG (in the presence of MPEP) also resulted in an increase in CREB phosphorylation in cultures derived from male animals (F = 67.87; **p < 0.01). D, E, Whole-cell recordings of female hippocampal neurons (n = 9) revealed that estradiol does not evoke glutamate release or alter the frequency of mEPSCs. Calibration: 50 pA, 25 ms. F, Estradiol increased CREB phosphorylation after the removal of extracellular calcium, further supporting the notion that estradiol activation of mGluR1a signaling is independent of presynaptic glutamate release. Error bars indicate SEM.