The parasubthalamic nucleus (PSTN) is activated by refeeding after food deprivation and several PSTN subpopulations have been shown to suppress feeding. However, no study to date directly addressed the role of PSTN neurons activated upon food access in the control of ensuing food consumption. Here we identify consumption latency as a sensitive behavioral indicator of PSTN activity, and show that, in hungry mice, the ensemble of refeeding-activated PSTN neurons drastically increases the latency to initiate refeeding with both familiar and a novel, familiar food, but does not control the amount of food consumed. In thirsty mice, this ensemble also delays sucrose consumption but accelerates water consumption, possibly reflecting anticipatory prandial thirst, with again no influence on the amount of fluid consumed. We next sought to identify which subpopulations of PSTN neurons might be driving these latency effects, using cell-type and pathway-specific chemogenetic manipulations. Our results suggest a prominent role of PSTN Tac1 neurons projecting to the central amygdala in the hindrance of feeding initiation. While PSTN Crh neurons also delay the latency of hungry mice to ingest familiar foods, they surprisingly promote the consumption of novel, palatable substances. Furthermore, PSTN Crh neurons projecting to the bed nucleus of the stria terminalis accelerate rehydration in thirsty mice. Our results demonstrate the key role of endogenous PSTN activity in the control of feeding and drinking initiation and delineate specific circuits mediating these effects, which may have relevance for eating disorders.

副底丘脑核 (PSTN) 在食物剥夺后通过重新进食而被激活，并且一些 PSTN 亚群已被证明可以抑制进食。然而，迄今为止，还没有研究直接探讨食物获取时激活的 PSTN 神经元在控制随后的食物消耗中的作用。在这里，我们将消耗潜伏期确定为 PSTN 活动的敏感行为指标，并表明，在饥饿的小鼠中，重新进食激活的 PSTN 神经元群大大增加了开始重新进食熟悉的食物和新的、熟悉的食物的潜伏期，但并不控制食物的摄入量。在口渴的小鼠中，这一整体也会延迟蔗糖的消耗，但会加速水的消耗，可能反映了预期的膳食口渴，但对液体消耗量没有影响。接下来，我们试图利用细胞类型和通路特异性化学遗传学操作来确定 PSTN 神经元的哪些亚群可能驱动这些潜伏效应。我们的结果表明，投射到中央杏仁核的 PSTN Tac1神经元在阻碍进食开始方面发挥着重要作用。虽然 PSTN Crh神经元也延迟了饥饿小鼠摄入熟悉食物的潜伏期，但它们令人惊讶地促进了新的、可口的物质的消耗。此外，投射到终纹床核的 PSTN Crh神经元可加速口渴小鼠的补液。我们的结果证明了内源性 PSTN 活性在控制进食和饮水起始中的关键作用，并描绘了介导这些作用的特定回路，这可能与饮食失调有关。