PDF(Pubmed)
Abstract：
Allostatic adaptations to a perceived threat are crucial for survival and may tap into mechanisms serving the homeostatic control of energy balance. We previously established that exposure to predator odor (PO) in rats significantly increases skeletal muscle thermogenesis and energy expenditure (EE). Evidence highlights steroidogenic factor 1 (SF1) cells within the central and dorsomedial ventromedial hypothalamus (c/dmVMH) as a modulator of both energy homeostasis and defensive behavior. However, the brain mechanism driving elevated EE and muscle thermogenesis during PO exposure has yet to be elucidated. To assess the ability of SF1 neurons of the c/dmVMH to induce muscle thermogenesis, we used the combined technology of chemogenetics, transgenic mice, temperature transponders, and indirect calorimetry. Here, we evaluate EE and muscle thermogenesis in SF1-Cre mice exposed to PO (ferret odor) compared to transgenic and viral controls. We detected significant increases in muscle temperature, EE, and oxygen consumption following the chemogenetic stimulation of SF1 cells. However, there were no detectable changes in muscle temperature in response to PO in either the presence or absence of chemogenetic stimulation. While the specific role of the VMH SF1 cells in PO-induced thermogenesis remains uncertain, these data establish a supporting role for SF1 neurons in the induction of muscle thermogenesis and EE similar to what is seen after predator threats.
摘要：
对感知到的威胁的异常适应对于生存至关重要，并且可能会利用用于能量平衡的稳态控制的机制。我们先前确定，大鼠暴露于捕食者气味（PO）会显着增加骨骼肌产热和能量消耗（EE）。证据强调了中央和背内侧腹下丘脑（c/dmVMH）中的类固醇生成因子1（SF1）细胞作为能量稳态和防御行为的调节剂。然而,在PO暴露期间驱动EE升高和肌肉产热的大脑机制尚未阐明。为了评估c/dmVMH的SF1神经元诱导肌肉产热的能力，我们使用了化学遗传学的组合技术，转基因小鼠，温度转发器,和间接量热法。这里,与转基因和病毒对照相比，我们评估暴露于PO（雪貂气味）的SF1-Cre小鼠的EE和肌肉产热。我们检测到肌肉温度显著升高，EE,和化学遗传刺激SF1细胞后的耗氧量。然而,在存在或不存在化学遗传刺激的情况下，响应PO的肌肉温度均无可检测到的变化。虽然VMHSF1细胞在PO诱导的产热中的具体作用仍不确定，这些数据建立了SF1神经元在诱导肌肉产热和EE中的支持作用，类似于捕食者威胁后看到的作用。
