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Results: 7

1.
Figure 3

Figure 3. Estradiol-induced EPSC potentiation and PPR decrease are input-specific. From: Estradiol acutely potentiates hippocampal excitatory synaptic transmission through a presynaptic mechanism.

EPSCs were evoked by alternating paired-pulse stimulation of two non-overlapping sets of Schaffer collateral inputs to a common CA1 pyramidal cell. A, A schematic of electrode placement and representative individual current traces evoked at E2-responsive and E2-nonresponsive inputs recorded from a single cell. B, Plot of mean ± SEM normalized EPSC amplitude (solid line) and PPR (dashed line) at E2-responsive inputs (green, n = 9); E2 decreased PPR in parallel with potentiating EPSCs in an input-specific manner; * indicates a significant effect of E2 on PPR, paired t-test: p<0.05. C, Plot of mean ± SEM normalized EPSC amplitude (solid line) and PPR (dashed line) at E2-nonresponsive inputs (blue) from the same cells as in (B). (See also Fig. S2.)

Tereza Smejkalova, et al. J Neurosci. ;30(48):16137-16148.
2.
Figure 7

Figure 7. Estradiol does not occlude the effect of paired-pulse facilitation to increase average cleft glutamate concentration. From: Estradiol acutely potentiates hippocampal excitatory synaptic transmission through a presynaptic mechanism.

EPSCs were evoked by paired-pulse stimulation (inter-pulse interval 50 ms). A, B, C, D, The low-affinity AMPAR antagonist γDGG (1 mM) was bath applied either in the absence or in the presence of E2 (100 nM). A, Representative individual traces recorded before and in γDGG in the absence of E2. B, Representative individual traces recorded before and in γDGG in the presence of E2. C, Plot of mean ± SEM normalized EPSC1 and EPSC2 amplitudes remaining in γDGG in the absence (n=6) vs. in the presence (n=9) of E2. Paired-pulse facilitation decreased the degree of EPSC block by γDGG similarly in the absence and presence of E2; two-way ANOVA: ** indicates a significant effect of EPSC number, p<0.01; and a significant effect of E2, p<0.01; interaction p>0.4. D, Plot of mean ± SEM PPR before and in γDGG in the absence (n=6) vs. in the presence (n=9) of E2. γDGG increased PPR similarly in the absence and presence of E2; two-way ANOVA: ** indicates a significant effect γDGG, p<0.01; * indicates a significant effect of E2, p<0.05; interaction p>0.7. E, F, G, H, The high-affinity AMPAR antagonist NBQX (200 nM) was bath applied either in the absence or in the presence of E2 (100 nM). E, Representative individual traces recorded before and in NBQX in the absence of E2. F, Representative individual traces recorded before and in NBQX in the presence of E2. G, Plot of mean ± SEM normalized EPSC1 and EPSC2 amplitudes remaining in NBQX in the absence (n=5) vs. in the presence (n=3) of E2. There was no significant difference. H, Plot of mean ± SEM PPR before and in NBQX in the absence (n=5) vs. in the presence (n=3) of E2. There was no significant difference.

Tereza Smejkalova, et al. J Neurosci. ;30(48):16137-16148.
3.
Figure 6

Figure 6. Estradiol increases average cleft glutamate concentration. From: Estradiol acutely potentiates hippocampal excitatory synaptic transmission through a presynaptic mechanism.

A, B, C, The low-affinity AMPAR antagonist γDGG (1 mM) was bath applied either in the absence or in the presence of E2 (100 nM). A, Representative experiment illustrating changes in EPSC amplitude during application of γDGG in the absence of E2. E2 was applied at the end of the experiment to confirm that the stimulated inputs were E2-responsive. Inset shows individual current traces from the same cell recorded in indicated conditions. B, Representative experiment illustrating changes in EPSC amplitude during application of γDGG in the presence of E2. Inset shows individual current traces from the same cell recorded in indicated conditions. C, Plot of normalized EPSC amplitude remaining in γDGG in the absence (n=6) vs. in the presence (n=9) of E2. γDGG was less effective in the presence of E2, consistent with higher average cleft glutamate concentration in E2; * indicates a significant effect of E2, t-test: p<0.05. D, E, F, The high-affinity AMPAR antagonist NBQX (200 nM) was bath applied either in the absence or in the presence of E2 (100 nM). D, Representative experiment illustrating changes in EPSC amplitude during application of NBQX in the absence of E2. E2 was applied at the end of the experiment to confirm that the stimulated inputs were E2-responsive. Inset shows individual current traces from the same cell recorded in indicated conditions. E, Representative experiment illustrating changes in EPSC amplitude during application of NBQX in the presence of E2. Inset shows individual current traces from the same cell recorded in indicated conditions. F, Plot of normalized EPSC amplitude remaining in NBQX in the absence (n=5) vs. in the presence (n=3) of E2. There was no significant difference. For C and F, open symbols represent individual experiments; filled symbols represent mean ± SEM in each condition.

Tereza Smejkalova, et al. J Neurosci. ;30(48):16137-16148.
4.
Figure 1

Figure 1. Estradiol acutely potentiates EPSC amplitude in a subset of experiments. From: Estradiol acutely potentiates hippocampal excitatory synaptic transmission through a presynaptic mechanism.

EPSCs evoked by Schaffer collateral pathway stimulation were recorded from CA1 pyramidal cells in acute slices from adult female rats (see Methods). Estradiol (E2, 100 pM – 100 nM) was bath applied for 10–15 min. A, Representative E2-responsive experiment illustrating the rapid time course of EPSC amplitude potentiation by E2. Inset shows a schematic of electrode placement and individual current traces recorded during baseline and in E2. B, Bimodal distribution of EPSC potentiation by E2 (100 nM) used to classify experiments as E2-responsive (> 20% increase; green) or E2-nonresponsive (≤ 20% increase; blue). C, Normalized EPSC amplitude in responders (green) and non-responders (blue) with various concentrations of 17β-E2 (100 pM – 100 nM) and 17α-E2 (100 nM). Each open symbol represents an individual experiment; filled symbols represent mean ± SEM for each condition. One-way ANOVA for normalized EPSC amplitude in E2-responsive experiments: p<0.01.

Tereza Smejkalova, et al. J Neurosci. ;30(48):16137-16148.
5.
Figure 5

Figure 5. Acute effects of estradiol on readily-releasable pool and individual vesicle release probability. From: Estradiol acutely potentiates hippocampal excitatory synaptic transmission through a presynaptic mechanism.

Size of the readily-releasable vesicle pool (RRP) and individual vesicle release probability (Pves) were estimated from responses to 100-pulse 20-Hz stimulus trains during baseline and in the presence of E2 (100 nM). A, Plot of mean ± SEM normalized EPSC charge during stimulus trains during baseline (black) and in 100 nM E2 (green) in E2-responsive experiments (n=12). Inset shows representative individual trace recorded during baseline. B, Representative individual traces evoked by the first 10 pulses of a 100-pulse stimulus train, before and in E2. C, Plot of mean ± SEM normalized EPSC charge during the first 10 pulses of 100-pulse stimulus trains during baseline and in 100 nM E2 (n=12). D, Plot of cumulative steady-state charge (sum of pulses 81–100) before and in E2. There was no significant difference. E, Plot of RRP charge ((sum of pulses 1–80) 4 ×(sum of pulses 81–100)) before and in E2; ** indicates a significant effect of E2, paired t-test: p<0.01. F, Plot of EPSC1 charge as proportion of RRP charge before and in E2. E2 consistently increased the proportion of RRP released by the first stimulus, consistent with increasing Pves; ** indicates a significant effect of E2, paired t-test: p<0.01. For D-F, connected open symbols represent individual experiments; filled symbols represent mean ± SEM in each condition. (See also Fig. S3.)

Tereza Smejkalova, et al. J Neurosci. ;30(48):16137-16148.
6.
Figure 2

Figure 2. Estradiol acutely increases release probability. From: Estradiol acutely potentiates hippocampal excitatory synaptic transmission through a presynaptic mechanism.

A, B, EPSCs were evoked by paired-pulse stimulation (inter-pulse interval 100 ms) before and during bath application of E2 (100 pM –100 nM). Experiments were classified as E2-responsive (green) or E2-nonresponsive (blue) based on >20% EPSC amplitude potentiation. A, Plot of mean ± SEM paired-pulse ratio (PPR) over time in E2-responsive experiments (n = 41). In E2-responsive experiments, PPR was high during baseline and decreased during E2 application; one-way ANOVA: p<0.01; ** indicates a significant difference between baseline PPR in E2-responsive vs. E2-nonresponsive experiments, t-test: p<0.01. Inset shows representative individual traces recorded during baseline and in E2. B, Plot of mean ± SEM PPR over time in E2-nonresponsive experiments (n = 39). In E2-nonresponsive experiments, PPR was relatively low during baseline and remained unchanged during E2 application; one-way ANOVA: p>0.7. Inset shows representative individual traces recorded during baseline and in E2. C, D, Effects of E2 were examined while AMPAR desensitization was blocked with cyclothiazide (CTZ). EPSCs were recorded before and during bath application of CTZ (100 μM), followed by bath application of CTZ (100 μM) + E2 (100 nM). C, Plot of mean ± SEM normalized EPSC amplitude (solid line) and PPR (dashed line) during baseline, in CTZ, and CTZ + E2 in E2-responsive experiments (n = 9). E2 acutely decreased PPR in parallel with potentiating EPSC amplitude even when AMPAR desensitization was blocked with CTZ; one-way ANOVA for EPSC amplitude: p<0.01; ** indicates a significant difference between CTZ and CTZ + E2, Bonferroni post-hoc test: p<0.01; one-way ANOVA for PPR: p<0.01; * indicates a significant difference between CTZ and CTZ + E2, Bonferroni post-hoc test: p<0.05. Inset shows representative individual traces recorded in indicated conditions. D, Plot of mean ± SEM normalized EPSC amplitude (solid line) and PPR (dashed line) during baseline, in CTZ, and CTZ + E2 in E2-nonresponsive experiments (n = 5). Inset shows representative individual traces recorded in indicated conditions. (See also Fig. S1.)

Tereza Smejkalova, et al. J Neurosci. ;30(48):16137-16148.
7.
Figure 4

Figure 4. Estradiol-induced EPSC potentiation and PPR decrease are mediated by ERβ and not ERα. From: Estradiol acutely potentiates hippocampal excitatory synaptic transmission through a presynaptic mechanism.

EPSCs were recorded during baseline and during bath application of estrogen receptor (ER)β-selective agonist DPN (100 or 500 nM) followed by E2 (100 nM), or during bath application of ERα-selective agonist PPT (100 or 200 nM) followed by E2 (100 nM), or during bath application of ER antagonist ICI 182,780 (100 nM) followed by E2 (100 nM). A, Representative experiment illustrating changes in EPSC amplitude during application of ERβ agonist DPN (500 nM), followed by E2 (100 nM). Inset shows representative individual traces from the same cell recorded in indicated conditions. B, Representative experiment illustrating changes in EPSC amplitude during application of ERα agonist PPT (100 nM), followed by E2 (100 nM). Inset shows representative individual traces from the same cell recorded in indicated conditions. C, Plot of mean ± SEM normalized EPSC amplitude during baseline, in DPN, and DPN + E2 in DPN-responsive (green, n = 8) and DPN-nonresponsive (blue, n=7) experiments. The ERβ agonist DPN mimicked and occluded EPSC potentiation by E2; one-way ANOVA for responders: p<0.01; ** indicates a significant difference between baseline and DPN, Bonferroni post hoc test: p<0.01. D, Plot of mean ± SEM normalized EPSC amplitude during baseline, in PPT, and PPT + E2 in E2-responsive (green, n = 5) and E2-nonresponsive (blue, n=3) experiments. In a subset of PPT-nonresponsive experiments, a subsequent response to E2 was observed; one-way ANOVA for responders: p<0.01; ** indicates a significant difference between PPT and PPT + E2, Bonferroni post hoc test: p<0.01. E, Plot of mean ± SEM normalized EPSC amplitude during baseline, in ICI 182,780, and ICI 182,780 + E2 in ICI-responsive (green, n = 4) and ICI-nonresponsive (blue, n=10) experiments. ICI 182,780 mimicked and occluded EPSC potentiation by E2; one-way ANOVA for responders: p<0.01; * indicates a significant difference between baseline and ICI 182,780, Bonferroni post hoc test: p<0.05. F, Plot of PPR in DPN-responsive experiments (n=12). DPN decreased PPR in parallel with potentiating EPSCs; ** paired t-test: p<0.01. G, Plot of PPR in DPN-nonresponsive experiments (n=11). There was no significant difference. H, Plot of PPR in all PPT experiments (n=15). There was no significant difference. I, Plot of PPR in ICI-responsive experiments (n=8). ICI 182,780 decreased PPR in parallel with potentiating EPSCs; * paired t-test: p<0.05. J, Plot of PPR in ICI-nonresponsive experiments (n=18). There was no significant difference. In F-J, connected open symbols represent individual experiments; filled symbols represent mean ± SEM in each condition.

Tereza Smejkalova, et al. J Neurosci. ;30(48):16137-16148.

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