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Fig. 3 | Molecular Brain

Fig. 3

From: G-protein coupled estrogen receptor (GPER1) activation promotes synaptic insertion of AMPA receptors and induction of chemical LTP at hippocampal temporoammonic-CA1 synapses

Fig. 3

GPER1-induced cLTP involves synaptic insertion of GluA2-lacking AMPA receptors. AC Plots of pooled data illustrating the effects on synaptic transmission at TA-CA1 synapses in juvenile hippocampal slices. A Application of G1 resulted in induction of cLTP, but prior exposure to philanthotoxin (Phtx; 1 µM; B) blocked G1-induced cLTP. C Application of philanthotoxin, 30 min after G1 failed to reverse the increase in synaptic efficacy induced by G1. Di Representative confocal images of surface GluA1 labelling in control hippocampal neurons (8–12 DIV) and after addition of G1, G15 and G1 plus G15. Dii Pooled data illustrating the relative effects on surface GluA1 immunolabelling in control neurons and after G1, G15, and G1 plus G15. G1 increases surface GluA1 expression via activation of GPER1. Ei Representative confocal images of surface GluA1 (green) and PSD-95 (red) labelling in control and G1 treated (DIV 8–13) neurons. G1 increases surface GluA1 that co-localises with PSD-95, indicating increased postsynaptic levels of GluA1. Eii, iii Pooled data indicating relative intensity of GluA1 (Eii) and % GluA1-PSD-95 co-localisation (Eiii) in control conditions and after G1 application. G1 increased GluA1 expression at hippocampal synapses

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