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. 2020 Jul 3;14:189. doi: 10.3389/fncel.2020.00189

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Copyright © 2020 Wang, Liang, Chen, Yau, Sun, Cheng, Xu, So and Li.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Adiponectin deficiency attenuates exercise-enhanced neurogenesis under stress. (A–C) COR treatment significantly lowered the number of BrdU⁺ newborn cells (A; n = 11–12 mice/group), Ki67⁺ proliferating cells (B; n = 9–15 mice/group) and DCX⁺ immature neurons (C; n = 9–15 mice/group) in both WT and ADN-KO mice. Voluntary exercise enhanced hippocampal neurogenesis by increasing all these three subsets of cells in COR-treated WT (WCR), but not ADN-null mice (KCR). Data are shown as means ± SD. **p < 0.01, ***p < 0.001 by two-way ANOVA and Tukey’s post hoc test. N.S., non-significant; BrdU, bromodeoxyuridine; Ki67, cell proliferation-associated nuclear antigen; DCX, doublecortin.