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. 2019 Jul 25;10:1738. doi: 10.3389/fimmu.2019.01738

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Copyright © 2019 DuBois, Ray, Gruber, Zhang, Aflakpui, Macian-Juan and Shafit-Zagardo.

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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Syn1-CKO mice have similar clinical outcomes to WT mice during MOG-induced EAE. (A) Confirmation of Akt3 knockdown in neurons. Free-floating cross-sections of brains isolated from Syn1-CKO and WT (Syn1Cre) mice immunostained with hematoxylin (top row) or Akt3 antibody (bottom row) and visualized by DAB. (B) Brain and spinal cords were isolated and weighed from naïve 8–10 week old sex-matched mice (n = 3/group) following perfusion with 1× PBS. (C) Syn1-CKO (n = 7) and WT (Akt3^fl/fl) (n = 5) mice were subjected to MOG-induced EAE. Mice were monitored daily for signs of clinical progression. No differences were observed between Syn1-CKO and WT over the course of a 23-day period following EAE induction. (D) From top to bottom, lumbar spinal cord sections from WT (Akt3^fl/fl) and Syn1-CKO were stained with H&E (top), SMI32, SMI99 (MBP), or Iba1 to assess axonal damage, demyelination, and microglia/macrophage levels, respectively.