Erratum: Slingshot-Cofilin activation mediates mitochondrial and synaptic dysfunction via Aβ ligation to β1-integrin conformers

Correction to: Cell Death and Differentiation (2015) 22, 921–934; doi:10.1038/cdd.2015.5; published online 20 February 2015

Since the publication of this paper, the authors have noticed the y-axis label of Figure 7e was incorrect. It should be % of the fESP slope. This has now been rectified and the corrected article appears in this issue together with this corrigendum.

Figure 7

Cofilin reduction rescues APP/Aβ-induced gliosis and loss of synaptic proteins as well as LTP and contextual memory deficits in APP/PS1 mice. (a and b) Seven-month-old WT, APP/PS1, and APP/PS1;Cofilin^+/− mice immunostained for GFAP, Synapsin I, and PSD95. (a) Representative images showing that Cofilin reduction ameliorates astrogliosis and synaptic damage associated with APP/PS1 mice. (b–d) Quantification of mean PSD95 and Synapsin I intensities in the stratum lucidum (SL; n=4 mice/genotype, 2 F and 2M, ANOVA, post hoc Tukey, *P<0.05, ^#P<0.0005). (c–e) Stimulating electrode placed in the Schaffer collaterals of the hippocampus and recording glass electrode positioned at the CA1 stratum radiatum below the pyramidal cell layer. (c) Input/output analysis generated by stepping up stimulation amplitude from 1 to 15 mV in WT, APP/PS1, and APP/PS1;Cofilin^+/− acute slices. No significant differences observed (n=24 slices from four mice, APP/PS1: 19 slices from four mice, APP/PS1;Cofilin^+/−: n=20 slices from three mice). (d) PPF showing no significant differences across genotypes and interstimulus interval except between APP/PS1;Cofilin^+/− and WT slices at the 40-ms interstimulus interval (two-way ANOVA, post hoc Bonferroni, *P<0.05; WT: n=32 slices from four mice, APP/PS1: n=31 slices from four mice, APP/PS1;Cofilin^+/−: n=25 slices from three mice). (e) LTP induced by the TBS showing significant differences in fEPSP slope in APP/PS1 compared with WT and APP/PS1;Cofilin^+/− slices (two-way ANOVA, post hoc Bonferroni, P<0.0001 at all time points). (WT: n=28 slices from four mice, APP/PS1: n=33 slices from four mice, APP/PS1;Cofilin^+/−: n=20 slices from three mice). Error bars represent S.E.M. (f) Percentage of time spent freezing during training period on day 1 (no significant differences observed by one-way ANOVA or Kruskal–Wallis statistic; WT n=12, APP/PS1 n=8, APP/PS1;Cofilin^+/− n=6; equal distribution of gender). Error bars represent S.E.M. (g) Percentage of time spend freezing during contextual fear conditioning (FC) on day 2 (Kruskal–Wallis statistic=9.66, P=0.008, genotypes=3, values=26; post hoc Dunn’s, *P<0.05; WTn=12, APP/PS1 n=8, APP/PS1;Cofilin^+/− n=6; equalized distribution of gender). (h) Percentage of time spent freezing during cued fear conditioning (FC) freezing on day 2 (no significant differences observed by one-way ANOVA or Kruskal–Wallis statistic; WT n=12, APP/PS1 n=8, APP/PS1;Cofilin^+/− n=6; equalized distribution of gender). (i) Total time spent on rotarod test (no significant differences observed by one-way ANOVA or Kruskal–Wallis statistic; WT n=11, APP/PS1 n=7, APP/PS1;Cofilin^+/− n=5; equalized distribution of gender). (j) Total distance traveled during open-field test (no significant differences observed by one-way ANOVA or Kruskal–Wallis statistic; WT n=11, APP/PS1 n=7, APP/PS1;Cofilin^+/− n=5; equalized distribution of gender). (k) Total time spent immobile during open-field test (no significant differences observed by 1-way ANOVA or Kruskal–Wallis statistic; WT n=11, APP/PS1 n=7, APP/PS1;Cofilin^+/− n=5; equalized distribution of gender)

The authors would like to apologize for any inconvenience this may have caused.