1 Department of Physiology, Hebei Medical University, Shijiazhuang 050017, Hebei, China 

2 Core Facilities and Centers, Institute of Medicine and Health, Hebei Medical University, Shijiazhuang 050017, Hebei, China 

3 School of Nursing, Hebei Medical University, Shijiazhuang 050000, Hebei, China 

4 Department of Orthodontics, College of Stomatology, Hebei Medical University, Shijiazhuang 050017, Hebei, China 

5 Hebei Key Laboratory of Neurophysiology, Shijiazhuang 050017, Hebei, China

 

Abstract

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 (NTSLepRb) neurons notably activated breathing. Moreover, stimulation of NTSLepRb 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 NTSLepRb neurons, but also activated LPBN neurons projecting to the preBo¨tzinger complex (preBo¨tC). By contrast, ablation of NTSLepRb neurons projecting to the LPBN notably eliminated the enhanced respiratory effect induced by NTSLepRb 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 NTSLepRb neurons. Therefore, leptin potentiates breathing in the NTS most likely via an NTS–LPBN–preBo¨tC circuit.

 

Keywords

Leptin; Ventilation; Nucleus tractus solitarii; Neural circuit; Chemogenetics

 

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