Lateral parabrachial FoxP2 neurons regulate respiratory responses to hypercapnia

被引:1
作者
Kaur, Satvinder [1 ,2 ]
Lynch, Nicole [1 ,2 ]
Sela, Yaniv [1 ,2 ]
Lima, Janayna D. [1 ,2 ]
Thomas, Renner C. [1 ,2 ]
Bandaru, Sathyajit S. [1 ,2 ]
Saper, Clifford B. [1 ,2 ]
机构
[1] Harvard Med Sch, Beth Israel Deaconess Med Ctr, Div Sleep Med, Dept Neurol, Boston, MA 02115 USA
[2] Harvard Med Sch, Beth Israel Deaconess Med Ctr, Program Neurosci, Boston, MA 02115 USA
关键词
FUNCTIONAL-ORGANIZATION; SLEEP; AROUSAL; NUCLEUS; COMPLEX; PARVALBUMIN; PROJECTIONS; ACTIVATION; MECHANISMS; MEDULLA;
D O I
暂无
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
About half of the neurons in the parabrachial nucleus (PB) that are activated by CO2 are located in the external lateral (el) subnucleus, express calcitonin gene-related peptide (CGRP), and cause forebrain arousal. We report here, in male mice, that most of the remaining CO2-responsive neurons in the adjacent central lateral (PBcl) and Kolliker-Fuse (KF) PB subnuclei express the transcription factor FoxP2 and many of these neurons project to respiratory sites in the medulla. PBcl(FoxP2) neurons show increased intracellular calcium during wakefulness and REM sleep and in response to elevated CO2 during NREM sleep. Photo-activation of the PBcl(FoxP2) neurons increases respiration, whereas either photo-inhibition of PBcl(FoxP2) or genetic deletion of PB/KFFoxP2 neurons reduces the respiratory response to CO2 stimulation without preventing awakening. Thus, augmenting the PBcl/KFFoxP2 response to CO2 in patients with sleep apnea in combination with inhibition of the PBel(CGRP) neurons may avoid hypoventilation and minimize EEG arousals.
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页数:17
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