Fig. 1: Stress activation of MeA neurons to regulate glucose.
From: Amygdala–liver signalling orchestrates glycaemic responses to stress
a, Schematic of the restraint stress condition. Created with BioRender (https://biorender.com/1ikn9ci). b, Blood glucose before and after no stress (control) or a 30 min restraint stress. c, Plasma corticosterone with (red) and without (grey) 30 min of restraint stress. d, Relative fold change in liver G6pc and Pck1 gene expression with (red) and without (grey) exposure to a 30 min restraint stress in sated mice. e, FOS expression in MeA at −1.58 mm from bregma in control and 30 min restrained mice. MeApd, posterior dorsal MeA; MeApv, posterior ventral MeA. Scale bar, 200 μm. f, Number of FOS+ cells in anterior (−1.06 mm to −1.34 mm from bregma) and posterior (−1.34 to −2.06 mm from bregma) MeA with (red) and without (grey) 30 min of restraint stress. g, Schematic of fibre photometry experiment (top) and image of GCaMP8s expression and fibre placement (bottom). Scale bar, 200 μm. ot, optic tract. h, z-score of GCaMP8s signal (bottom) and blood glucose (top) before, during and after 30 min of restraint stress in MeA. Bars along the top indicate capture (pink), restraint (red) and release (grey). i, GCaMP8s z-score aligned to start of the capture period. j, Mean GCaMP8s z-score for 5 min baseline, 30 s capture, 30 min restraint and 5 min release periods. k, Schematic of MeA chemogenetic activation and MeA expression of hSyn-hM3DGq-mCherry. l,m, Blood glucose in mice treated as depicted in k, with CNO (3 mg kg−1, intraperitoneal injection) and fasted for 6 h, without (l) and with (m) metyrapone pretreatment at −60 min relative to CNO injection. n,o, Plasma corticosterone (n) and insulin (o) in mice treated as depicted in k, with CNO (3 mg kg−1, intraperitoneal injection) and fasted for 6 h. Data are mean ± s.e.m. Individual data points represent individual mice. Sample size and statistical analyses in Supplementary Data Table 1.
