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. 2017 May 5;55(4):3185–3195. doi: 10.1007/s12035-017-0565-8

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© The Author(s) 2017

Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

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Fig. 1 — CSPG impairs NSC penetration into the injury site after TBI and acts through NgR. a Two-week postinjury glial scar was already formed and NSC migration was evaluated. DCX+ neuroblasts (green) leave their niche at the lateral ventricle (LV) and migrate towards the injury site characterized by high expression of CSPG (magenta). NSC are prevented to enter the proteoglycan-rich regions, accumulate at the injury border, and migrate around this area (detail). Scale bar at 100 μm. b NSC cultured as neurospheres were plated on laminin + CS with or without the NgR inhibitor NEP1–40. CS inhibits NSC migration and decreases the distance traveled by the cells. In the presence of NEP1–40, NSC migrated longer distances (p < 0.0001), suggesting that the inhibition of migration promoted by CS is mediated by NgR. Data were collected 18 h after neurospheres were plated. Number of neurospheres analyzed: with NEP1–40 = 115; without NEP1–40 = 123. NSC were immunolabeled with GFAP (green) and nuclei stained with DAPI. Scale bar at 200 μm (Color figure online)