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. 2020 May 11;11:351. doi: 10.3389/fphys.2020.00351

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Copyright © 2020 Zhao, Shang, Wang, Xie and Liu.

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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Fluoxetine ameliorated neuronal injury and behavioral changes resulting from up-regulation of p38 in DG. (A) Schematics of AAV vectors engineered to overexpress p38 or eGFP control. (B) Illustration of bilateral viral injection of AAV–p38 in DG. (C) Validation of the efficient overexpression of p38 in DG. (D) Fluoxetine prevented the morphological changes in microglia and astrocytes within the DG (AP, –3.35 mm from bregma) caused by p38 overexpression. (E) Fluoxetine reduced Iba1 and GFAP levels in DG. (F) Fluoxetine reduced the increased levels of pro-apoptotic factors caused by p38 overexpression in DG. (G) Fluoxetine reduced immobility times. (H) Fluoxetine increased sucrose solution consumption. For behavioral tests, N = 18 per group. For other experiments, N = 6 per group. *p < 0.05, **p < 0.01 compared to the control group; ^#p < 0.05, ^##p < 0.01 compared to the CUMS group.