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. 2017 Jun 19;7:3809. doi: 10.1038/s41598-017-03680-2

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as 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 images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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l-SPD selectively activates mTOR signaling by D1R agonism rather than D2R antagonism. One week cultured primary cortical neurons were incubated with drugs for 4 hours. (A) Western blot images and (D) quantification analysis of pmTOR (Ser 2448), mTOR, GluR1 in the treatment of vehicle, l-SPD (10 µM or 50 µM), SCH23390 (10 µM) and SCH23390 (10 µM) with l-SPD (10 µM or 50 µM). (B) Western blot images and (E) quantification analysis of pmTOR (Ser 2448), mTOR, GluR1 in the treatment of vehicle, l-SPD (10 µM or 50 µM), Quinpirole (10 µM) and Quinpirole (10 µM) with l-SPD (10 µM or 50 µM). (C) Western blot images and (F) quantification analysis of pmTOR (Ser 2448), mTOR, GluR1 in the treatment of vehicle, l-SPD (10 µM or 50 µM), H89 (10 µM) and H89 (10 µM) with l-SPD (10 µM or 50 µM). The β-tubulin were determined as reference protein. *p < 0.05, compared to the vehicle treatment group. ^# p < 0.05, compared to the 50 µM l-SPD treatment group.