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. 2022 Mar 18;12:4741. doi: 10.1038/s41598-022-08615-0

Author Correction: Adrenergic inhibition facilitates normalization of extracellular potassium after cortical spreading depolarization

Hiromu Monai 1,2,, Shinnosuke Koketsu 3, Yoshiaki Shinohara 3,4, Takatoshi Ueki 3, Peter Kusk 5, Natalie L Hauglund 5, Andrew J Samson 5, Maiken Nedergaard 5,6, Hajime Hirase 1,5,
PMCID: PMC8933480  PMID: 35304562

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.

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.


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