Divergent neurocircuitry dissociates two components of the stress response: glucose mobilization and anxiety-like behavior

This is the authors' abstract. We don't add key points for this paper.

Stress is a risk factor for emotion and energy metabolism disorders. However, the neurocircuitry mechanisms for emotion initiation and glucose mobilization underlying stress responses are unclear. Here we demonstrate that photoactivation of Gad2+ projection from the anterior bed nucleus of the stria terminalis (aBNST) to the arcuate nucleus (ARC) induces anxiety-like behavior as well as acute hyperglycemia. Photoinhibition of the circuit is anxiolytic and blocks hyperglycemia induced by restraint stress. Pharmacogenetic inhibition of the ARC Gad2+ →raphe obscurus nucleus (ROb) and photoactivation of the aBNST Gad2+ →ARC circuits simultaneously leads to significant hypoglycemia and anxiety-like behavior. Pharmacogenetic inhibition of the ARC Gad2+ →nucleus of the solitary tract (NTS) whilst photoactivation of the aBNST Gad2+ →ARC circuit only induces hyperglycemia. Our results reveal that the aBNST Gad2+ →ARC Gad2+ →ROb circuit is recruited for the stress response of rapid glucose mobilization and the aBNST Gad2+ →ARC Gad2+ →NTS circuit for behavioral symptoms of stress response. This study identifies a possible general strategy for neurocircuitry structural organization dealing with multiple organs involved in responses, with potential therapeutic targets for emotion and energy metabolism disorders underlying psychiatric disorders.