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. 2020 Oct 21;10:17921. doi: 10.1038/s41598-020-74496-w

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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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Roles of CP-AMPAR in NMDAR-dependent LTD. (a) Left; Dose response relationship of D-AP5 and NASPM on LFS-induced LTD (IC₅₀ and Hill’s coefficient; D-AP5, 0.35 µM and 0.78 ± 0.1, n = 3; NASPM, 0.1 µM and 0.92 ± 0.1, n = 3). Right; Treatment with both DAP5 (0.35 μM) and NASPM (0.1 μM) completely inhibited LTD induction in the LHb (97.4 ± 3.2%, n = 6). (b) NASPM failed to inhibit LFS-induced LTD in aCSF containing low Mg²⁺ (0.5 mM) and glycine (10 μM) (LFS-LTD, 77.9 ± 3.9%, n = 5). (c) Chemically NMDA-induced LTD was induced in the LHb after 15 min of treatment with NMDA (30 μM)(76.9 ± 2.2%, n = 6) and was completely inhibited by NASPM (20 μM)(96.3 ± 2.5%, n = 6) and by ifenprodil (10 μM)(98.6 ± 2.6%, n = 4). (d) NASPM did not block chemically NMDA-induced LTD (65.5 ± 5.6%, n = 5).