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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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Function of CP-AMPAR and NMDAR for the induction of extrasynaptic LTD in the LHb. (a) Left; While the application of ( +)MK-801 (3 μM) completely suppressed LFS-induced LTD (95.1 ± 1.4%, n = 6), LFS steadily induced extrasynaptic LTD after the application of DL-TBOA (10 μM) (81.0 ± 4.0%, n = 6). Right; After the treatment of DL-TBOA without LFS, the change of amplitude showed a significant potentiation five minutes after the drug application of DL-TBOA but did not lead to the change of fEPSP slope. (b) LFS-induced LTD completely inhibited by the co-application of DL-TBOA with NASPM (20 μM; 97.5 ± 3.3%, n = 3), NVPAAM 077 (0.1 μM; 100.6 ± 1.7%, n = 5), ifenprodil (0.1 μM; 100.6 ± 1.7%, n = 5). However, the coapplication of DL-TBOA with LY367385 (100 μM) did not show any inhibitory effects on LFS-induced LTD (74.1 ± 3.7%, n = 3). (c) After MK-801 exposure, chemically NMDA-induced LTD was generated in aCSF containing low Mg²⁺ (0.5 mM) and glycine (10 μM) (69.9 ± 2.0%, n = 2).