Circadian Timekeeping of Body Temperature by the Mammalian Suprachiasmatic Nucleus
type: CreativeWork
description: The circadian rhythm of body temperature (CRT) is a universal cue for entraining the peripheral clocks in mammals. The hypothalamic suprachiasmatic nucleus (SCN) is required for generating the ~24-hour rhythms of body temperature (Tb); however, the neural mechanism underlying this regulation remains poorly understood. Here, we searched for circadian clocks in the SCN that are necessary for maintaining CRT in mice using a stepwise loss-of-function genetic approach and radiotelemetry recordings. We show that genetic deletion of Bmal1, a non-redundant clock gene for driving the cell-autonomous circadian clock, broadly in the forebrain inclusive of the SCN sufficiently abolished the circadian rhythmicity of Tb. In contrast, genetic deletion of Bmal1 specifically from the neuromedin s (Nms)-expressing neurons in the SCN progressively impaired CRT over the course of a month in constant darkness. Interestingly, synaptic inhibition of a subpopulation of these Nms neurons co-expressing arginine vasopressin lengthened the circadian period of CRT. Finally, local chemogenetic inhibition of the SCN Nms neurons prevented hypothermia specifically during the late subjective night and sustained until subjective dawn, but not at other circadian times of a day. Together, our findings unveiled a role of the SCN Nms neurons in the circadian modulation of Tb with a hypothermic role manifested at late night, possibly to prepare the nocturnal mice for rest in the day.
abstract: The circadian rhythm of body temperature (CRT) is a universal cue for entraining the peripheral clocks in mammals. The hypothalamic suprachiasmatic nucleus (SCN) is required for generating the ~24-hour rhythms of body temperature (Tb); however, the neural mechanism underlying this regulation remains poorly understood. Here, we searched for circadian clocks in the SCN that are necessary for maintaining CRT in mice using a stepwise loss-of-function genetic approach and radiotelemetry recordings. We show that genetic deletion of Bmal1, a non-redundant clock gene for driving the cell-autonomous circadian clock, broadly in the forebrain inclusive of the SCN sufficiently abolished the circadian rhythmicity of Tb. In contrast, genetic deletion of Bmal1 specifically from the neuromedin s (Nms)-expressing neurons in the SCN progressively impaired CRT over the course of a month in constant darkness. Interestingly, synaptic inhibition of a subpopulation of these Nms neurons co-expressing arginine vasopressin lengthened the circadian period of CRT. Finally, local chemogenetic inhibition of the SCN Nms neurons prevented hypothermia specifically during the late subjective night and sustained until subjective dawn, but not at other circadian times of a day. Together, our findings unveiled a role of the SCN Nms neurons in the circadian modulation of Tb with a hypothermic role manifested at late night, possibly to prepare the nocturnal mice for rest in the day.
author: Liao, I-Mei
language: en
keywords: Circadian Clocks, Circadian Rhythm, Neurons, Neuropeptides, Suprachiasmatic Nucleus
date published: 2025-01-02T21:57:54Z
date modified: 2026-07-24T05:52:17Z
provider: University of Texas Southwestern Medical Center
publisher: Networked Digital Library of Theses and Dissertations
type: WebPage
source organization: University of Texas Southwestern Medical Center

PropertyValue
property ID: Handle
value: https://hdl.handle.net/2152.5/10449