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. 2019 Nov 20;5:797–808. doi: 10.1016/j.trci.2019.10.003

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© 2019 The Authors

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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Fig. 4 — AβOs abolished LTP-associated GluA1 exocytosis in both PSLM and non-PSLM. (A) Representative GluA1-SEP (green) exocytosis (arrows) in PSLM or non-PSLM (left), and the time courses of GluA1-SEP signal intensity (right) before and after the exocytosis (0 sec). PSD95-RFPt (magenta) was recorded before the stimulation and merged with time-lapse images of GluA1-SEP. The signal increased rapidly and then decreased gradually by lateral diffusion and photo-bleaching. (B) Images of GluA1-SEP and PSD95-RFPt before and after the stimulation (left), and kymographs of GluA1-SEP signals (middle). GluA1 exocytosis occurred in both PSLM (white arrows) and non-PSLM (white arrowheads), particularly 1 min after the stimulation (black arrows). Frequencies of GluA1-SEP exocytosis in PSLN (red, left ordinate) and non-PSLM (black, right ordinate) before and after the stimulation (right). (C) Statistical analyses of data in (B). Significant differences between revAβ and AβOs (Benjamin-Hochberg test), or before and after the stimulation (Dunnett's test) are indicated by asterisks (N = 23, 23 cells, *P < .05, **P < .01, ***P < .001). (D) The intensity of the GluA1-SEP signal in each exocytosis in PSLM and non-PSLM before and after the stimulation. No significant difference was detected by Dunnett's test.