Leptin, an adipocyte-derived peptide hormone, has been shown to facilitate breathing. However, the central sites and circuit mechanisms underlying the respiratory effects of leptin remain incompletely understood. The present study aimed to address whether neurons expressing leptin receptor b (LepRb) in the nucleus tractus solitarii (NTS) contribute to respiratory control. Both chemogenetic and optogenetic stimulation of LepRb-expressing NTS (NTS^LepRb) neurons notably activated breathing. Moreover, stimulation of NTS^LepRb neurons projecting to the lateral parabrachial nucleus (LPBN) not only remarkably increased basal ventilation to a level similar to that of the stimulation of all NTS^LepRb neurons, but also activated LPBN neurons projecting to the preBötzinger complex (preBötC). By contrast, ablation of NTS^LepRb neurons projecting to the LPBN notably eliminated the enhanced respiratory effect induced by NTS^LepRb neuron stimulation. In brainstem slices, bath application of leptin rapidly depolarized the membrane potential, increased the spontaneous firing rate, and accelerated the Ca²⁺ transients in most NTS^LepRb neurons. Therefore, leptin potentiates breathing in the NTS most likely via an NTS–LPBN–preBötC circuit.

瘦素是一种脂肪细胞衍生的肽激素，已被证明可以促进呼吸。然而，瘦素呼吸作用背后的中心部位和回路机制仍未完全了解。本研究旨在探讨在孤束核 (NTS) 中表达瘦素受体 b (LepRb) 的神经元是否有助于呼吸控制。表达 LepRb 的 NTS (NTS ^LepRb ) 神经元的化学遗传学和光遗传学刺激都显着激活了呼吸。此外，刺激投射到臂旁外侧核 (LPBN) 的 NTS ^LepRb神经元不仅显着增加基础通气量，达到与所有 NTS ^{LepRb刺激相似的水平。}神经元，但也激活了投射到 preBötzinger 复合体 (preBötC) 的 LPBN 神经元。相比之下，投射到 LPBN 的 NTS ^LepRb神经元的消融显着消除了 NTS ^LepRb神经元刺激诱导的增强呼吸效应。在脑干切片中，瘦素的浴应用使膜电位迅速去极化，增加了自发放电率，并加速了大多数 NTS ^LepRb神经元中的 Ca ^2+瞬变。因此，瘦素最有可能通过NTS-LPBN-preBötC 回路增强 NTS 中的呼吸。