A Central Catecholaminergic Circuit Controls Blood Glucose Le

AAVs of tracing helper and RV were used for retrograde monosynaptic tracing. (From BrainVTA)

The viruses used from BrainVTA in this article are in the table below

Tracing Helper	AAV-DIO-TVA-EGFP AAV-DIO-G
RV	Rabies viruses SAD-OG-mCherry(EnvA)

Zhe Zhao, Liang Wang, Wenling Gao, Fei Hu, Juen Zhang, Yuqi Ren, Rui Lin, Qiru Feng, Mingxiu Cheng, Dapeng Ju, Qingsheng Chi, Dehua Wang, Sen Song, Minmin Luo, Cheng Zhan
Pub Date: 2017-11-05, DOI: 10.1016/j.neuron.2017.05.031, Email: sales@brainvta.com

Stress-induced hyperglycemia is a fundamental adaptive response that mobilizes energy stores in response to threats. Here, our examination of the contributions of the central catecholaminergic (CA) neuronal system to this adaptive response revealed that CA neurons in the ventrolateral medulla (VLM) control stress-induced hyperglycemia. Ablation of VLM CA neurons abolished the hyperglycemic response to both physical and psychological stress, whereas chemogenetic activation of these neurons was sufficient to induce hyperglycemia. We further found that CA neurons in the rostral VLM, but not those in the caudal VLM, cause hyperglycemia via descending projections to the spinal cord. Monosynaptic tracing experiments showed that VLM CA neurons receive direct inputs from multiple stress-responsive brain areas. Optogenetic studies identified an excitatory PVN-VLM circuit that induces hyperglycemia. This study establishes the central role of VLM CA neurons in stress-induced hyperglycemia and substantially expands our understanding of the central mechanism that controls glucose metabolism.

Figure 1. The VLM Catecholaminergic Neuronal Population Plays a Central Role in Controlling LPS-Induced Hyperglycemia.

In the study, the authors used a cell-type-speciﬁc ablation approach to survey the roles of three different populations (LC, NTS, and VLM) of central CA neurons in stress-induced hyperglycemia. They identiﬁed a neural circuit that controls blood glucose levels during stress. They demonstrate that VLM CA neurons integrate stress signals from multiple stress-related areas (e.g., the PVN) and cause hyperglycemia via descending projections to the spinal cord.

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