Figure 8.
SNX17 and SNX27 promote the recycling of different cargoes upon cLTP. (A) Representative confocal images of surface β1-integrin levels of DIV17 hippocampal neurons that were infected at DIV11 with lentiviruses carrying either ctrl-, SNX17-, or SNX27-shRNAs. Neurons were treated in the presence or absence of cLTP and live labeled with an anti-surface β1-integrin antibody for 15 min, followed by fixation and immunostaining for MAP2. Scale bar, 5 µm. (B) The mean intensity of β1-integrin in the first 50 µm of secondary dendrites was quantified, and values were normalized to crtl-shRNA. ctrl-shRNA: 1,000 ± 0.025, N = 40 neurons; ctrl-shRNA cLTP: 1.168 ± 0.034, N = 40 neurons; SNX17-shRNA: 0.720 ± 0.034, N = 40 neurons; SNX17-shRNA cLTP: 0.725 ± 0.046, N = 40 neurons; SNX27-shRNA: 1.003 ± 0.036, N = 40 neurons; SNX27-shRNA cLTP: 1.191 ± 0.028, N = 40 neurons. Three independent experiments. Data were analyzed by one-way ANOVA with Tukey’s post hoc test, **P < 0.01. Error bars are SEM. (C) Representative confocal images of surface GluA1 levels of DIV17 hippocampal neurons that were infected at DIV11 with lentiviruses carrying either ctrl-, SNX17-, or SNX27-shRNAs. Neurons were treated in the presence or absence of cLTP and live labeled with an anti-surface GluA1 antibody for 15 min, followed by fixation and immunostaining for MAP2. Scale bar, 5 µm. (D) The mean intensity of surface GluA1 in the first 50 µm of secondary dendrites was quantified, and values were normalized to crtl-shRNA. ctrl-shRNA: 1,000 ± 0.025, N = 40 neurons; ctrl-shRNA cLTP: 1.135 ± 0.033, N = 40 neurons; SNX17-shRNA: 0.946 ± 0.031, N = 40 neurons; SNX17-shRNA cLTP: 1.097 ± 0.035, N = 40 neurons; SNX27-shRNA: 0.757 ± 0.033, N = 40 neurons; SNX27-shRNA cLTP: 0.706 ± 0.025, N = 40 neurons. Three independent experiments. Data were analyzed by one-way ANOVA with Tukey’s post hoc test, *P < 0.05, **P < 0.01. Error bars are SEM. DIV, days in vitro.

SNX17 and SNX27 promote the recycling of different cargoes upon cLTP. (A) Representative confocal images of surface β1-integrin levels of DIV17 hippocampal neurons that were infected at DIV11 with lentiviruses carrying either ctrl-, SNX17-, or SNX27-shRNAs. Neurons were treated in the presence or absence of cLTP and live labeled with an anti-surface β1-integrin antibody for 15 min, followed by fixation and immunostaining for MAP2. Scale bar, 5 µm. (B) The mean intensity of β1-integrin in the first 50 µm of secondary dendrites was quantified, and values were normalized to crtl-shRNA. ctrl-shRNA: 1,000 ± 0.025, N = 40 neurons; ctrl-shRNA cLTP: 1.168 ± 0.034, N = 40 neurons; SNX17-shRNA: 0.720 ± 0.034, N = 40 neurons; SNX17-shRNA cLTP: 0.725 ± 0.046, N = 40 neurons; SNX27-shRNA: 1.003 ± 0.036, N = 40 neurons; SNX27-shRNA cLTP: 1.191 ± 0.028, N = 40 neurons. Three independent experiments. Data were analyzed by one-way ANOVA with Tukey’s post hoc test, **P < 0.01. Error bars are SEM. (C) Representative confocal images of surface GluA1 levels of DIV17 hippocampal neurons that were infected at DIV11 with lentiviruses carrying either ctrl-, SNX17-, or SNX27-shRNAs. Neurons were treated in the presence or absence of cLTP and live labeled with an anti-surface GluA1 antibody for 15 min, followed by fixation and immunostaining for MAP2. Scale bar, 5 µm. (D) The mean intensity of surface GluA1 in the first 50 µm of secondary dendrites was quantified, and values were normalized to crtl-shRNA. ctrl-shRNA: 1,000 ± 0.025, N = 40 neurons; ctrl-shRNA cLTP: 1.135 ± 0.033, N = 40 neurons; SNX17-shRNA: 0.946 ± 0.031, N = 40 neurons; SNX17-shRNA cLTP: 1.097 ± 0.035, N = 40 neurons; SNX27-shRNA: 0.757 ± 0.033, N = 40 neurons; SNX27-shRNA cLTP: 0.706 ± 0.025, N = 40 neurons. Three independent experiments. Data were analyzed by one-way ANOVA with Tukey’s post hoc test, *P < 0.05, **P < 0.01. Error bars are SEM. DIV, days in vitro.

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