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. 2019 Oct 23;10:4814. doi: 10.1038/s41467-019-12736-y

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© The Author(s) 2019

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 — Altered thalamocortical FFI in P10–11 Fmr1-KO mouse. a Left: Trial-averaged voltage-clamp recordings showing direct thalamocortical EPSCs and FF-IPSCs from an example Fmr1^+/Y Layer 4 SC, Scale: 25 ms/500 pA. The strength of TC-FFI (“G/A ratio”) is quantified as the ratio of peak evoked current. Right: Strength of TC-FFI at P10–11. Points indicate neurons, bars are mean ± SEM. Unlike for Fmr1^+/Y recordings (28 neurons, max. 3 per animal), in Fmr1^−/Y neurons, some cells (8/38 neurons, max. 3 per animal) lacked FFI; light red bars indicate FFI strength of cells with G/A > 0, hollow markers. Including Fmr1^−/Y neurons with G/A = 0, average strength of FFI was not significantly different to that of Fmr1^+/Y, but excluding these neurons (dark red bars and solid markers), the average strength was elevated over that of FFI in wild-type recordings (Fmr1^+/Y vs. all Fmr1^−/Y neurons: p = 0.40, Fmr1^+/Y vs. Fmr1^−/Y neurons with G/A > 0: p = 0.005, Mann–Whitney). b Synaptic kinetics of currents underlying TC-FFI. Left: Example TC-evoked currents in from Fmr1^+/Y (blue) and Fmr1^−/Y (red), EPSCs and FF-IPSCs, individually scaled to peak amplitudes. Note the slower decay time constant and onset latency for Fmr1^−/Y FFI-PSCs (indicated by red and blue arrows). Right: Slower FFI synaptic kinetics for Fmr1^−/Y SCs. No significant genotype-dependent differences were observed in the same comparisons for kinetics of EPSCs. Asterisks indicate p < 0.05 (t-test), N’s (neurons): 23 Fmr1^+/Y/26 Fmr1^−/Y (EPSCs); 27 Fmr1^+/Y/28 Fmr1^−/Y (FF-IPSCs). c Example TC EPSPs from SCs receiving low, medium and high TC-FFI. Note the progressive curtailment of EPSP duration with increasing FFI strength, the lack of a Fmr1^+/Y example for G/A = 0, and the exaggerated IPSP for the high strength FFI Fmr1^−/Y example. d Slower TC EPSPs in Fmr1^−/Y. Full width at half-height (‘half-width’) of EPSPs from SCs (N (neurons) = 19 Fmr1^+/Y, 36 Fmr1^−/Y), bars are mean ± SEM, asterisks denote p < 0.05 (t-test). Not shown: the dependence of Fmr1-KO thalamocortical EPSP duration on the strength of FFI is distorted. Fmr1-KO Neurons with weaker/no FFI (G/A ratio < 2) showed specifically broadened EPSP duration (22.4 ± 7.30 ms vs. 68.4 ± 16 ms, Fmr1^+/Y vs. Fmr1^−/Y, p = 0.02), whereas this effect was dampened in neurons with stronger FFI (13.2 ± 8.70 ms vs. 37.1 ± 15.8 ms, Fmr1^+/Y vs. Fmr1^−/Y, p = 0.07)