Abstract
Neural signals play a critical role in metabolic regulation by controlling behavior and coordinating glucose production and uptake in peripheral organs. Physiological and psychological stimuli that disrupt homeostasis - stressors - result in metabolic and behavioral adaptations but our understanding of the precise circuits underlying these adaptations remains incomplete. Here we used in vivo calcium imaging, viral tracing and neural manipulation to determine the contribution of medial amygdala (MeA) circuits to the metabolic responses to stress. Social and psychological stressors result in hyperglycemia. These stressors also rapidly increased fluorescence of genetic calcium indicators (GCamp) in MeA neurons. Chemogenetic activation of MeA neurons significantly increased blood glucose without altering pancreatic hormone release and suppressed feeding. Viral tracing revealed distinct MeA subpopulations projecting to the bed nucleus of the stria terminalis (BNST) and to the ventromedial hypothalamus (VMH) . Chemogenetic stimulation of MeA projections to the VMH but not BNST increased blood glucose during glucose tolerance testing via sympathetic activation of hepatic gluconeogenesis, without effects on pancreatic or adrenal hormones. Conversely, silencing of MeA neurons projecting to the VMH blunted stress-induced hyperglycemia. Together these findings suggest a crucial role for MeA circuits in the metabolic response to stressors with dissociation of sympathetic, hormonal, and behavioral adaptations to homeostatic challenge. Disclosure K.Devarakonda: None. R.O’connor: None. A.Alvarsson: None. R.Y.Li: None. M.Jimenez gonzalez: None. P.Kenny: None. S.Stanley: None. Funding American Diabetes Association (1-17-ACE-31) ; National Institutes of Health (R01NS097184, OT2OD024912, F31DK129016 and R01DK124461) National Science Foundation (1930163) Department of Defense (W81XWH-20-1-0156, W81XWH-20-1-0345) Naomi Berries Diabetes Center Russell Berrie Foundation AwardRevson Foundation
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