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A Neural Circuit Mechanism Controlling Breathing by Leptin in the Nucleus Tractus Solitarii

作     者:Hongxiao Yu Luo Shi Jinting Chen Shirui Jun Yinchao Hao Shuang Wang Congrui Fu Xiang Zhang Haiyan Lu Sheng Wang Fang Yuan Hongxiao Yu;Luo Shi;Jinting Chen;Shirui Jun;Yinchao Hao;Shuang Wang;Congrui Fu;Xiang Zhang;Haiyan Lu;Sheng Wang;Fang Yuan

作者机构:Department of PhysiologyHebei Medical UniversityShijiazhuang 050017HebeiChina Core Facilities and CentersInstitute of Medicine and HealthHebei Medical UniversityShijiazhuang 050017HebeiChina School of NursingHebei Medical UniversityShijiazhuang 050000HebeiChina Department of OrthodonticsCollege of StomatologyHebei Medical UniversityShijiazhuang 050017HebeiChina Hebei Key Laboratory of NeurophysiologyShiji azhuang 050017HebeiChina 

出 版 物:《Neuroscience Bulletin》 (神经科学通报(英文版))

年 卷 期:2022年第38卷第2期

页      面:149-165页

核心收录:

学科分类:0710[理学-生物学] 07[理学] 1001[医学-基础医学(可授医学、理学学位)] 071006[理学-神经生物学] 

基  金:supported by the National Natural Science Foundation of China(31800981 and 31971058) the Natural Science Foundation of Hebei Province for Distinguished Young Scholars(H2020206509) a Hebei Province Government Grant(CXZZBS2020119). 

主  题:Leptin Ventilation Nucleus tractus solitarii Neural circuit Chemogenetics 

摘      要: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-ex-pressing 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 preBotzinger complex(preBotC).By contrast,ablation of NTS^pRb 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-preBdtC circuit.

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