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. 2016 Nov 22;5:e19334. doi: 10.7554/eLife.19334

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© 2016, Murphy et al

This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited.

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Figure 7. — (A) 20G03^GAL4 drives mCD8-GFP expression in neurons with cell bodies positioned proximal to cell arborizations of those labeled by Lkr^GAL4. (B) Overlaid images of 20G03^GAL4 and Lkr^GAL4 expression show close proximity between cell types in the lateral horn and SOG. (C) Overexpression of Kir^2.1 channel in 20G03^GAL4-labeled cells results in an enhanced postprandial sleep response (30 flies per genotype, n = 805 meals, Kir^2.1/ w¹¹¹⁸; 488, 20G03^GAL4 / w¹¹¹⁸; 285, Kir^2.1/ 20G03^GAL4; **p<0.01; ***p<0.001, Kruskal-Wallis test followed by Dunn’s multiple comparisons). (D) Conditional silencing of 20G03^GAL4-labeled cells in adulthood is sufficient to increase postprandial sleep (24 flies per genotype, n = 493 meals, Tub^GAL80ts; Kir^2.1/ w^CS; 575, 20G03^GAL4 / w^CS; 528, Tub^GAL80ts; Kir^2.1/20G03^GAL41; *p<0.05; **p<0.01, Kruskal-Wallis test followed by Dunn’s multiple comparisons). (E) Time-course of postprandial sleep reveals that effect of 20G03^GAL4 silencing is most prominent from ZT 10–14 (time-course partitioned into 4 hr bins, shaded region indicates dark period; *p<0.05, Kruskal-Wallis test followed by Dunn’s multiple comparisons). (F) Conditional silencing effects are also stronger at dusk ZT 10–14 (**p<0.01, Kruskal-Wallis test followed by Dunn’s multiple comparisons). (G) Comparison of P_sleep in the 20 min before and after each meal for both 20G03^GAL4 manipulations (color codes from C and D; *p<0.05; **p<0.01, ***p<0.001, Kruskal-Wallis test followed by Dunn’s multiple comparisons). (H) Proposed model for regulation of postprandial sleep by dietary components and neuronal circuitry. Meal volume, ingested salt, and protein drive postprandial sleep. Sleep induced by ingested protein acts through Lkr neurons. Protein also induces a waking response independent of Lkr neuronal activity. Leucokininergic (Lk) or non-leucokininergic (20G03) cell populations can independently inhibit postprandial sleep, possibly through modulation of Lkr neuronal activity.

DOI: http://dx.doi.org/10.7554/eLife.19334.018

Figure 7—figure supplement 1. — (A) 20G03^GAL4 drives mCD8-GFP expression in neurons with cell bodies positioned proximal to cell arborizations of those labeled by Lkr^GAL4. (B) Overlaid images of 20G03^GAL4 and Lkr^GAL4 expression show close proximity between cell types in the lateral horn and SOG. (C) Overexpression of Kir^2.1 channel in 20G03^GAL4-labeled cells results in an enhanced postprandial sleep response (30 flies per genotype, n = 805 meals, Kir^2.1/ w¹¹¹⁸; 488, 20G03^GAL4 / w¹¹¹⁸; 285, Kir^2.1/ 20G03^GAL4; **p<0.01; ***p<0.001, Kruskal-Wallis test followed by Dunn’s multiple comparisons). (D) Conditional silencing of 20G03^GAL4-labeled cells in adulthood is sufficient to increase postprandial sleep (24 flies per genotype, n = 493 meals, Tub^GAL80ts; Kir^2.1/ w^CS; 575, 20G03^GAL4 / w^CS; 528, Tub^GAL80ts; Kir^2.1/20G03^GAL41; *p<0.05; **p<0.01, Kruskal-Wallis test followed by Dunn’s multiple comparisons). (E) Time-course of postprandial sleep reveals that effect of 20G03^GAL4 silencing is most prominent from ZT 10–14 (time-course partitioned into 4 hr bins, shaded region indicates dark period; *p<0.05, Kruskal-Wallis test followed by Dunn’s multiple comparisons). (F) Conditional silencing effects are also stronger at dusk ZT 10–14 (**p<0.01, Kruskal-Wallis test followed by Dunn’s multiple comparisons). (G) Comparison of P_sleep in the 20 min before and after each meal for both 20G03^GAL4 manipulations (color codes from C and D; *p<0.05; **p<0.01, ***p<0.001, Kruskal-Wallis test followed by Dunn’s multiple comparisons). (H) Proposed model for regulation of postprandial sleep by dietary components and neuronal circuitry. Meal volume, ingested salt, and protein drive postprandial sleep. Sleep induced by ingested protein acts through Lkr neurons. Protein also induces a waking response independent of Lkr neuronal activity. Leucokininergic (Lk) or non-leucokininergic (20G03) cell populations can independently inhibit postprandial sleep, possibly through modulation of Lkr neuronal activity.

DOI: http://dx.doi.org/10.7554/eLife.19334.018