A Neural Circuit Mechanism Controlling Breathing by Leptin in the Nucleus Tractus Solitarii.
10.1007/s12264-021-00742-4
- Author:
Hongxiao YU
1
;
Luo SHI
1
;
Jinting CHEN
2
;
Shirui JUN
1
;
Yinchao HAO
1
;
Shuang WANG
1
;
Congrui FU
3
;
Xiang ZHANG
1
;
Haiyan LU
4
;
Sheng WANG
5
;
Fang YUAN
6
Author Information
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. Department of Physiology, Hebei Medical University, Shijiazhuang, 050017, Hebei, China. wangsheng@hebmu.edu.cn.
6. Department of Physiology, Hebei Medical University, Shijiazhuang, 050017, Hebei, China. yuanfphy@163.com.
- Publication Type:Journal Article
- Keywords:
Chemogenetics;
Leptin;
Neural circuit;
Nucleus tractus solitarii;
Ventilation
- MeSH:
Leptin/pharmacology*;
Membrane Potentials;
Neurons/metabolism*;
Solitary Nucleus/metabolism*
- From:
Neuroscience Bulletin
2022;38(2):149-165
- CountryChina
- Language:English
-
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 preBötzinger complex (preBötC). 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-preBötC circuit.
