Fig. 6: NTD conformations determine GluA2 mobility at the synapse.
a, Fluorescence recovery over time for GluA2 wt–SEP or GluA2F231A–SEP expressed in dissociated hippocampal neurons, imaged at either pH 7.4 or pH 5.5. Normalized data were fit to a single exponential curve (time constant of fit: GluA2 pH 7.4, τ = 87 s (n = 12 cells from three culture preparations); GluA2 pH 5.5, τ = 100 s (n = 11); GluA2F231A pH 7.4, τ = 114 s (n = 12); GluA2F231A pH 5.5, τ = 96 s (n = 9)). Overlapping fluorescence recovery profiles for dendritic regions are shown in gray. The insets present example images with the dendrite outlined in white and the 2-µm2 region of the spine imaged boxed in red. Scale bar, 2 µm. b. Fluorescence recovery 630 s after bleaching (GluA2 pH 7.4 = 0.44 ± 0.03 (n = 12 cells from three culture preparations), GluA2 pH 5.5 = 0.66 ± 0.03 (n = 11), GluA2F231A pH 7.4 = 0.63 ± 0.04 (n = 12) and GluA2F231A pH 5.5 = 0.60 ± 0.02 (n = 9). Statistical differences were determined by a one-way ANOVA. ****P < 0.0001 and ***P = 0.0007. c. Schematic depicting protonation of the GluA2 BD NTD (red) interface following presynaptic vesicle release, resulting in splaying of the GluA2 NTD and subsequent diffusion of desensitized receptors away from the release site (right) allowing renewal of the receptor population by resting or activatable receptors (left).
