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. 2023 Jun 22;42(6):892–904. doi: 10.1038/s41587-023-01833-5

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© The Author(s) 2023

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. 6 — a, Vagal electrophysiology during intestinal optofluidic modulation. b, Duodenal sucrose (300 mM) increases vagal firing rate. c, Quantification of peak responses (n = 4; *P = 0.0304 by Kruskal–Wallis test with nonparametric comparisons using Wilcoxon method). d, Optogenetic stimulation of Cck⁺ cells increases vagal firing rate. e, Quantification of peak responses; *P < 0.0367 by Kruskal–Wallis test with nonparametric comparisons using Wilcoxon method, baseline (n = 5) versus blue µLED (n = 5): P = 0.0367; baseline versus green µLED (n = 4): P = 0.1113; blue µLED versus green µLED: P = 0.0200. f,g, Schematic of wireless intraduodenal optogenetic control of Cck⁺ cells (f) while evaluating feeding behavior (g). h,i, Chow intake in (h) Cck::ChR2 mice (n = 4, significant effect of time (P = 0.0003), stimulation (P < 0.0001) and time × stimulation interaction (P = 0.0086); post hoc two-sided paired t-tests: 1 h, P = 0.0161; 2 h, P = 0.0376; 3 h, P = 0.0044) and for (i) control mice lacking ChR2 (n = 4, significant effect of time (P = 0.0020), but not stimulation (P = 0.4975) or time × stimulation interaction (P = 0.8906)). j,k, Illustration of ileal optogenetic control of Pyy⁺ cells (j) while evaluating food intake (k). l, Ensure intake for Pyy::ChR2 mice during wireless optical stimulation (n = 4, significant effect of time (P < 0.0001), stimulation (P < 0.0001) and time × stimulation interaction (P < 0.0001)). m, Cumulative intake of l (two-sided paired t-test, P = 0.0381). n, Ensure intake for control mice (n = 4 mice, significant effect of time (P < 0.0001) and stimulation (P = 0.0160), but no significant time × stimulation interaction (P = 0.5796)). o, Cumulative intake for n (two-sided paired t-test, P = 0.4639). p, Schematic of brain VTA electrophysiology during duodenal microfluidic infusion. q, Firing rate of a putative DA neuron is sensitive to quinpirole. r, Intraduodenal sucrose increases firing rate of putative DA neurons compared with saline (saline: n = 20; sucrose: n = 18 neurons; two-sided Wilcoxon signed-rank test, P = 0.8595, P = 6.71387 × 10⁻⁴, respectively). s, Schematic of duodenal optogenetic stimulation in Phox2b::ChR2 mice. t,u, Percentage preference at baseline and on test day for Phox2b::ChR2 (t) and control mice lacking ChR2 (u) (two-sided paired t-test, Phox2b::ChR2: P = 0.014, t = 4.19, d.f. = 4; control mice: P = 0.110, t = –2.25, d.f. = 3). v,w, Representative heat-maps of animal position corresponding to t (v) and u (w). All data are represented as mean ± s.e.m, except in r which shows mean ± s.d. Ephys, electrophysiology.

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