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. 2018 Oct 8;9:4118. doi: 10.1038/s41467-018-06409-5

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© The Author(s) 2018

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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Fig. 4 — eCB-tLTP does not depend on D₂R expressed by D₂R-MSNs. a Location of D₂R in striatum expressed in striato-pallidal MSNs, cholinergic interneurons, SNc dopaminergic and cortical glutamatergic afferents. Right: the two complementary strategies to identify the D₂R involved in eCB-tLTP: (1) genetic-ablation of D₂R-MSN or cholinergic interneurons (using DTR and stereotaxic DT injection) and 6-ODHA-ablation of dopaminergic cells in the MFB, and (2) D₂R-cKO in D₂R-MSN, cholinergic interneurons, dopaminergic cells, or corticostriatal glutamatergic afferents; NA accounts for the impossibility to use a genetic-ablation of corticostriatal afferents without losing the studied EPSCs. b, c tLTP induced with 15 post-pre pairings is observed in both striato-nigral (D₁R-eGFP positive neurons, D₁R-eGFP⁺, n = 6, 5/6 cells showed tLTP) (b) and striato-pallidal (D₁R-eGFP negative neurons, non-D₁R-eGFP⁺, n = 7, 7/7 cells showed tLTP) (c) MSNs. d, e Experiments of plasticity expression in genetically-ablated mice for A₂A-expressing neurons in the dorsal striatum. d In situ hybridization autoradiograms (left) and quantification (right bar graph, n = 5 mice) of enkephalin mRNA in striatum caudal level of coronal sections in A_2A-Cre^+/−::iDTR^+/−::Drd1a-GFP^+/− mice injected with DT stereotaxically in the dorsal striatum (right hemisphere) and without DT injection (left hemisphere). Scale bars: 1000 µm. e In mice in which D₂R-MSNs were ablated (A_2A-Cre^+/−::iDTR^+/−::Drd1a-GFP^+/− mice injected with DT stereotaxically in the dorsal striatum) tLTP was induced with 15 post-pre pairings (n = 7, 7/7 cells showed tLTP). f, g Experiments of plasticity expression in selective cKO for D₂R expressed by striatal D₂R-MSNs. f In mice in which D₂R was specifically knocked-out in D₂R-MSNs (A_2A-Cre^+/−::Drd2^LoxP/LoxP mice) tLTP was induced with 15 post-pre pairings (n = 6, 5/6 cells showed tLTP). g tLTP was observed in mice serving as the Cre driver control (A_2A-Cre^+/−::Drd2^Wt/Wt mice, n = 7, 6/7 cells showed tLTP). Representative traces are the average of 15 EPSCs during baseline (black traces) and 45 min after STDP protocol (grey traces). Vertical grey dashed line indicates the STDP protocol. Error bars represent sem. *p < 0.05; **p < 0.01; ***p < 0.001 by one sample t-test (b, c–g) or Wilcoxon Signed rank test (b)