Extended Data Fig. 10: Activity of IPCs was stimulated by sNPF application, and the circulating trehalose level in which CN neurons had beeninactivated was reduced.

a, b, Average GCaMP traces (a) and ΔF/F (max) quantifications (b) from the IPCs in response to 80 µM sNPF in AHL or DMSO in AHL. c, An increase in circulating trehalose level in fed or starved flies in which CN neurons were inactivated. The levels of circulating trehalose in flies carrying CN-Gal4 and UAS-Kir2.1 and its heterozygote controls (CN-Gal4/+ and UAS-Kir2.1/+). d, A working model of the anatomic connectivities between CN neurons and IPCs (green), and between CN neurons and AKH-producing cells (red). CN neurons regulate glucose homeostasis by counter-balancing the activities of IPCs and AKH-producing cells through sNPF neurotransmitter that activates IPCs and inactivates AKH-producing cells. *P < 0.05, **P < 0.01 and ***P < 0.001; unpaired two-tailed t-test (b) and one-way ANOVA with Tukey post hoc test (c). See Supplementary Table 1 for the sample sizes and statistical analyses.