Brainstem catecholaminergic neurons induce torpor during fasting by orchestrating cardiovascular and thermoregulation changes.

Abstract

Torpor, an adaptive hypometabolic state in response to fasting, is characterized by pronounced reductions in body temperature, heart rate, and thermogenesis. However, how the brain orchestrates these physiological changes to induce torpor and the relationships among them remain elusive. Inhibiting catecholaminergic (CA) neurons in the ventrolateral medulla (VLM) significantly impairs torpor in mice, while their activation reduces body temperature, heart rate, energy expenditure, physical activity, and thermogenesis. Importantly, the heart rate decline precedes body temperature reduction, resembling patterns observed in natural torpid animals. Moreover, a likely causal relationship exists between heart rate reduction and body temperature decline. VLM-CA neurons may regulate heart rate and thermogenesis through projections to the dorsal motor vagal nucleus and medial preoptic area, respectively. Additionally, these neurons are conserved in Daurian ground squirrels and become active before hibernation, indicating their potential role in hibernation. Here, we find that VLM-CA neurons play important roles in fasting-induced torpor.