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. 2018 Nov 9;9:4724. doi: 10.1038/s41467-018-07113-0

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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. 7 — Electrophysiological properties of inhibitory (FSNs) and excitatory neurons in the PTC of GM6001-treated mice. a Unaltered resting membrane potential (Vm) of FSNs in the PTC of GM6001-treated (62.88 ± 1.40, n = 18(5)) than in nontreated (GBM22) PTC (61.67 ± 1.01, n = 12(8)), but significantly different than in sham (69.85 ± 0.67, n = 7(6)). b Lower Cm of FSNs in the PTC of GM6001-treated (28.27 ± 1.36, n = 20(5)) than nontreated (43.84 ± 3.74, n = 13(8)), but similar to sham (30.11 ± 1.99, n = 15(6)). c Unaltered R_in of FSNs in GM6001-treated PTC (219.90 ± 15.69, n = 20(5)) compared to GBM22 PTC (249.10 ± 17.65, n = 13(9)) and sham (252.64 ± 35.30, n = 13(7)). d Threshold current of FSNs remained unaltered in GM6001-treated PTC (120.76 ± 8.96, n = 13(5)) compared to nontreated PTC (82.75 ± 11.49, n = 8(6)) and sham (87.25 ± 16.06, n = 8(5)). e Higher AP frequency of FSNs in GM6001-treated PTC (n = 12(5)) than in nontreated PTC (n = 18(11)) but not than in sham (n = 10(7)). f Representative Vm traces from nontreated (upper) and GM6001-treated PTC (lower) FSNs on −100pA (black) and 140pA (red) current steps. g Resting membrane potential (Vm) of excitatory neurons in GM6001-treated PTC (66.62 ± 0.77, n = 27(8)) remained similar to sham (67.02 ± 0.38, n = 98(15)), but was significantly higher than the nontreated PTC (61.49 ± 0.86, n = 80(11)). h Cm of excitatory neurons in GM6001-treated PTC remained unaltered (PTC, 72.90 ± 8.92, n = 17(10); GM6001-treated PTC, 67.00 ± 6.95, n = 26(8); sham, 73.93 ± 6.95, n = 27(10)). i Input resistance (R_in) of excitatory neurons in GM6001-treated PTC (244.64 ± 9.24, n = 27(6)) was not significantly different than in nontreated PTC (288.18 ± 15.82, n = 23(10)), but than in sham (298.63 ± 14.47, n = 39(10)). j Lower threshold current in excitatory neurons in nontreated PTC (134.76 ± 14.69, n = 13(8)) than in GM6001-treated PTC (138.75 ± 6.81, n = 24(8)) and sham (171.33 ± 5.28, n = 39(10)). k Higher AP (firing) frequency of excitatory neurons in GM6001-treated PTC (n = 25(5)) than in nontreated PTC (n = 27(10)) and in sham (n = 36(10)). l Representative Vm traces from nontreated PTC (upper) and GM6001-treated PTC (lower) excitatory neurons on −100pA and 60pA current steps. n = cells(mice) in all. The units for membrane potential (Vm), threshold current, membrane capacitance (Cm) and input resistance (R_in) are mV, pA, pF, and MΩ, respectively. ****P < 0.0001, ***P < 0.001, **P < 0.01, *P < 0.05, one-way ANOVA in (a−d, g−j); two-way ANOVA in (e, k) (GM6001-treated vs. nontreated); Tukey's post-hoc test in all. ####P < 0.0001, ###P < 0.001, ##P < 0.01, #P < 0.05, two-way ANOVA, Tukey’s post-hoc test in (k) (GM6001-treated vs. sham)