.png){kind=icon}
.png){kind=icon}
Return
Graphical abstract
.png){kind=icon}
OA
AI
DOI：10.1016/j.neuron.2022.08.027.png)
.png){kind=icon}
Original request for help.png){kind=icon}
Share.png){kind=icon}
Save
Abstract
En 中文
Sleep disturbances are strongly associated with cardiovascular diseases. Baroreflex, a basic cardiovascular regulation mechanism, is modulated by sleep-wake states. Here, we show that neurons at key stages of bar-oreflex pathways also promote sleep. Using activity-dependent genetic labeling, we tagged neurons in the nucleus of the solitary tract (NST) activated by blood pressure elevation and confirmed their barosensitivity with optrode recording and calcium imaging. Chemogenetic or optogenetic activation of these neurons pro-moted non-REM sleep in addition to decreasing blood pressure and heart rate. GABAergic neurons in the caudal ventrolateral medulla (CVLM)-a downstream target of the NST for vasomotor baroreflex-also pro-mote non-REM sleep, partly by inhibiting the sympathoexcitatory and wake-promoting adrenergic neurons in the rostral ventrolateral medulla (RVLM). Cholinergic neurons in the nucleus ambiguous-a target of the NST for cardiac baroreflex-promoted non-REM sleep as well. Thus, key components of the cardiovascular bar-oreflex circuit are also integral to sleep-wake brain-state regulation.
Keywords:
BLOOD-PRESSURE
BARORECEPTOR REFLEX
ARTERIAL-PRESSURE
BAROSENSITIVE NEURONS
SYMPATHETIC OUTFLOW
TRACTUS-SOLITARIUS
C1 NEURONS
SLEEP
AROUSAL
STIMULATION
Journal
IF:
15
Papers:
1.4W
Citations:
9.9W
