Correction to: Scientific Reports 10.1038/s41598-021-87609-w, published online 14 April 2021
The original version of this Article contained errors in Figure 3 (B) and (C), where grey shadings were incorrectly positioned.
The original Figure 3 and accompanying legend appear below.
Figure 3.
CSD propagation and neural activity recovery in IP3R2 KO mice. (A) Representative image of the time series of CSD propagation. Other than using IP3R2−/−;G7NG817wt/tg double transgenic mouse as subjects, the experimental conditions are the same as in Fig. 1. Scale bar 1 mm. (B) Example trace of Ca2+ activity of an ROI located ~ 2 mm anterior to the KCl application site (Black square indicated in A). Note that neural activity does not recover completely within 50 min. (C) Similar Ca2+ signal trace as (B). measured in an IP3R2−/−;G7NG817wt/tg mouse pretreated with AdR blockers. (D) Comparison of CSD Ca2+ wave number during 10 min KCl application between IP3R2+/−;G7NG817wt/tg and IP3R2−/−:G7NG817wt/tg mice. 1.8 ± 0.2 vs. 1.6 ± 0.3, from N = 10 vs. N = 8, p = 0.64. (E) Comparison of CSD Ca2+ propagation speed between IP3R2+/−;G7NG817wt/tg and IP3R2−/−:G7NG817wt/tg mice. First wave: 4.2 ± 0.2 vs. 4.5 ± 0.1 mm/min; second wave: 5.5 ± 1.4 vs. 3.1 ± 0.2 mm/min. (F) Comparison of CSD Ca2+ wave duration between IP3R2+/−;G7NG817wt/tg and IP3R2−/−;G7NG817wt/tg mice. First wave: 49.3 ± 5.4 vs. 50.9 ± 8.0 s; second wave: 35.0 ± 3.8 vs. 37.4 ± 11.6 s. (G) Comparison of inter-CSD Ca2+ wave interval between IP3R2+/−;G7NG817wt/tg and IP3R2−/−;G7NG817wt/tg mice. 353.5 ± 20.9 s vs. 386.6 ± 57.1 s, N = 6 vs. N = 4, p = 0.54. (H) Comparison of first and second CSD Ca2+ wave onset time between IP3R2+/−;G7NG817wt/tg (WT, black) and IP3R2−/−;G7NG817wt/tg (IP3R2 KO, blue) mice. First wave: 38.3 ± 2.6 vs. 45.0 ± 3.2 s, N = 10 vs. N = 8; second wave: 391.4 ± 22.1 vs. 434.3 ± 59.5 s, N = 7 vs. N = 4. (I) Comparison of baseline amplitude before AdR blocker in IP3R2−/−;G7NG817wt/tg mice. (J) Effect of AdR blocker pretreatment on the recovery of neural oscillations after KCl-induced CSD in IP3R2−/−;G7NG817wt/tg mice. Recovery is facilitated by AdR blocker pretreatment (N = 6) compared with the untreated control group (N = 6). (K,L) Comparisons of mean somatic and gliopil Ca2+ probability in IP3R2 KO expressing G-CaMP7 in astrocytes via AAV (I, 80 cells vs. 113 cells from N = 3 mice) and gliopil Ca2+ events in IP3R2 KO mice (J, N = 3 mice). *p < 0.05.
The original Article has been corrected.
Contributor Information
Hiromu Monai, Email: monai.hiromu@ocha.ac.jp.
Hajime Hirase, Email: hirase@sund.ku.dk.

