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. 2020 Jan 17;10:608. doi: 10.1038/s41598-020-57484-y

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© The Author(s) 2020

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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Inhibition of RSK reduced the 5-HT-induced phosphorylation of CREB1 and reduced LTF. (A) BID, a RSK inhibitor, blocked 5-HT-induced increases in pCREB1. (A1) Protocol for BID application with 5-HT or Veh. (A2) Representative confocal images of pCREB1 in SNs 2 h after treatment. (A3) Summary data. 5-HT-induced increase in pCREB1 was blocked by pre-incubation with BID (n = 6 independent experiments). Scale bar, 20 μm. (B) BID attenuated LTF. (B1) Protocol for BID application with 5-HT or Veh and EPSP recording. (B2) Representative EPSPs recorded immediately before (pre) and 24 h after treatment with 5-HT or Veh. Dashed lines represent the amplitude of the pre-test EPSPs. (B3) Summary data. Application of BID significantly reduced LTF produced by the S protocol (Veh, n = 7; 5-HT, n = 8; BID, n = 7; BID + 5-HT, n = 7).