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. 2020 Mar 11;26(6):1860–1879. doi: 10.1038/s41380-020-0686-8

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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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Fig. 3 — a Experimental timeline. Representative image of ChR2-eYFP expression in the VH (left) and NAc (right) of D1-tdtomato mice. b, h Paired pulse ratio is unaffected by conditioned fear in D1-MSNs (n = 8 per group; two-way ANOVA; treatment main effect; F_{(2, 18)} = 0.06, p = 0.9388; ISI main effect; F_{(2, 36)} = 3.44, p < 0.043; treatment × intensity interaction; F_{(4, 36)} = 2.21, p = 0.087) and D2-MSNs (n = 6 controls; n = 9 footshock stress; two-way ANOVA; treatment main effect; F_{(2, 18)} = 0.37, p = 0.6983; ISI main effect; F_{(2, 36)} = 0.53, p = 0.5917; treatment × intensity interaction; F_{(4, 36)} = 0.07, p = 0.9912). c, i Biophysically-isolated AMPA-R/NMDAR in D1-MSNs (left; blue) and D2-MSNs (right; red) in mice in the tone (white), and footshock (light color) groups. D1-MSNs (n = 14–15 cells per group; t-test; t₍₂₇₎ = 4.26, p = 0.0002). D2-MSNs (n = 8–9 per group; t-test; t₍₁₅₎ = 0.03, p = 0.98). Pharmacologically isolated AMPA-R/NMDAR in D1-MSNs and D2-MSNs. D1-MSNs (n = 8–9 per group; t-test; t₍₁₅₎ = 3.24, p = 0.0055). D2-MSNs (n = 8 per group; t-test; t₍₁₄₎ = 0.15, p = 0.88). d, j Increased VH AMPAR oEPSCs in D1-MSNs from mice in the footshock group relative to the tone group (n = 7–9 per group; two-way ANOVA; treatment × intensity; F_{(6, 84)} = 8.2, p < 0.0001). VH AMPAR oEPSC input curves in D2-MSNs are not significantly different between tone and footshock groups (n = 6–8 per group; two-way ANOVA; treatment main effect; F_{(1, 12)} = 0.12, p = 0.73; Intensity main effect; F_{(6, 72)} = 34.26, p < 0.0001; Treatment × intensity interaction; F_(6,72) = 0.44, p = 0.85). e, k No difference in VH NMDAR oEPSCs in D1-MSNs (n = 7–8 per group; two-way ANOVA; treatment main effect; F_{(1, 13)} = 1.48, p = 0.2449; intensity main effect; F_{(6, 78)} = 63.61, p < 0.0001; treatment × intensity interaction; F_(6,78) = 0.79, p = 0.5811), and D2-MSNs between footshock and tone groups (n = 5–9 per group; two-way ANOVA; treatment main effect; F_{(2, 19)} = 0.25, p = 0.7798; intensity main effect; F_{(6, 114)} = 68.1, p < 0.0001; treatment × intensity interaction; F_{(12, 114)} = 0.24, p = 0.9957). f, l Current–voltage curves of VH AMPAR oEPSCs. D1-MSNs (n = 8–11 per group; Two-way ANOVA; treatment main effect; F_{(1, 17)} = 0.002, p = 0.96; voltage main effect; F_{(2, 34)} = 566.99, p < 0.0001; treatment × voltage interaction; F_{(2, 34)} = 0.2, p = 0.82). D2-MSNs (n = 8–10 per group; two-way ANOVA; treatment main effect; F_{(1, 16)} = 0.15, p = 0.70; voltage main effect; F_{(2, 32)} = 1241.32, p < 0.0001; treatment × voltage interaction; F_{(2, 32)} = 0.56, p = 0.58). g, m Current–voltage curves of VH NMDAR oEPSCs. D1-MSNs (n = 10 per group; two-way ANOVA; treatment main effect; F_{(1, 18)} = 2.14, p = 0.16; voltage main effect; F_(6,108) = 244.69, p < 0.0001; treatment × voltage interaction; F_(6,108) = 1.36, p = 0.24). D2-MSNs (n = 8–10 per group; two-way ANOVA; treatment × voltage interaction; F_(6,96) = 2.37, p = 0.035).