Fig. 1

GPER1 activation results in a persistent increase in excitatory synaptic transmission. Ai, Bi. Representative experiment showing effects of estrogen (1 µM; 15 min) on excitatory synaptic transmission at TA-CA1 synapses in juvenile male hippocampal slices. Application of E2 resulted in a persistent increase in excitatory synaptic transmission (Ai) that was blocked by the GPER1 antagonist, G15 (Bi). At the end of experiments, addition of dopamine (100 µM; 5 min) inhibits synaptic transmission, confirming stimulation of TA input. Aii–Bii, Plots of pooled data demonstrating that E2 increases synaptic efficacy (Aii) and this effect is blocked by G15 (Bii). In this and subsequent figures, each point is the average of four successive responses and representative fEPSPs are shown above each plot and for the time indicated. C, D Plots of pooled data demonstrating that addition of the GPER1 agonist, G1 (10 nM; 15 min) resulted in a persistent increase in synaptic transmission at TA-CA1 synapses (C) but was without effect at SC-CA1 synapses (D). Note the lack of effect of dopamine at SC-CA1 synapses. E, F Pooled data showing that the effects of G1 are due to activation of GPER1 as G1 effects were blocked by the selective GPER1 antagonists, G15 (200 nM; E) and G36 (1 µM; F)