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. 2018 Oct 1;18:268. doi: 10.1186/s12906-018-2330-6

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© The Author(s). 2018

Open AccessThis 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. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 2 — B-TCE pretreatment suppressed the neuronal degeneration induced by glutamate by modulating the expression of neuronal structural markers. a) Confocal micrographs of Control, Glutamate (2 mM), B-TCE (20 μg/mL) and B-TCE + Glu treated primary cerebellar neurons immunostained for MAP-2, GAP-43 and NF200. b) Representative immunoblots for MAP-2, GAP-43 and NF200 where α-Tubulin was used as internal control. c) Histogram representing relative expression of MAP-2 (i), GAP-43 (ii) and NF200 (iii) obtained from normalized relative optical densities of bands. Data was compared between Control and other groups such as Glutamate, B-TCE and B-TCE + Glu (^*p ≤ 0.01) as well as Glutamate alone with B-TCE and B-TCE + Glu groups (^#p ≤ 0.01). Confocal Images were captured at 60X objective (Scale bar: 50 μm)