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Fig. 3 | Molecular Brain

Fig. 3

From: A new mouse line with reduced GluA2 Q/R site RNA editing exhibits loss of dendritic spines, hippocampal CA1-neuron loss, learning and memory impairments and NMDA receptor-independent seizure vulnerability

Fig. 3

AMPAR-mediated excitatory synaptic transmission and long-term synaptic plasticity in CA1 hippocampal neurons. a Averaged traces of AMPA evoked EPSCs at − 70 and + 40 mV in WT and GluA2+/ECS(G) mice. b Current-voltage (I/V) relationship of synaptic responses at − 70, 0 and + 40 mV in WT and GluA2+/ECS(G) mice (n=10 GluA2+/ECS(G) and 15 WT cells, normalized to evoked EPSC amplitude at − 70 mV; t-test). c Time plot of evoked EPSC amplitude in the presence of the Ca2+-permeable AMPAR antagonist, Naspm (50 μM, n=7 GluA2+/ECS(G) and 8 WT cells), normalized to the pre-Naspm baseline. Inset: Representative current traces of AMPA EPSCs (recorded at − 70 mV) before and during application of Naspm in WT and GluA2+/ECS(G) mice. HFS induced LTP of fEPSPs in the hippocampal CA1 region of GluA2+/ECS(G) and WT mice, in (d) control ACSF (n=5 GluA2+/ECS(G) and 7 WT slices; t-test), and in the presence of (e) the NMDA receptor antagonist DL-AP5 (100 μM; n=7 GluA2+/ECS(G) and 6 WT slices; t-test), or (f) DL-AP5 plus the Ca2+-permeable AMPAR antagonist IEM1460 (50 μM; n=5 GluA2+/ECS(G) and 6 WT slices; t-test). In (df) fEPSP slope is normalized over 20 min prior to HFS. g Kainate induced Co2+ loading in the hippocampus revealed Co2+ uptake in the CA1 cell layer of GluA2+/ECS(G) mice. h The AMPA and Kainate receptor antagonist NBQX (20 μM), and the non-competitive AMPAR antagonist GYKI 52466 (100 μM) sufficiently blocked Co2+ update in the CA1

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