scholarly journals The Suprachiasmatic Nucleus, Circadian Clocks, and the Liver

Diabetes ◽  
2013 ◽  
Vol 62 (4) ◽  
pp. 1017-1019 ◽  
Author(s):  
J. M. Radziuk
Keyword(s):  
Suprachiasmatic Nucleus ◽  
Circadian Clocks

scholarly journals Impairment of Peripheral Circadian Clocks Precedes Metabolic Abnormalities in ob/ob Mice

Endocrinology ◽  
2011 ◽  
Vol 152 (4) ◽  
pp. 1347-1354 ◽  
Author(s):  
Hitoshi Ando ◽  
Masafumi Kumazaki ◽  
Yuya Motosugi ◽  
Kentarou Ushijima ◽  
Tomohiro Maekawa ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Suprachiasmatic Nucleus ◽  
Expression Profiles ◽  
Circadian Clocks ◽  
Metabolic Abnormalities ◽  
Peripheral Tissues ◽  
Low Calorie Diet ◽  
Leptin Deficiency ◽  
Calorie Diet ◽  
Peripheral Clocks

Abstract Recent studies have demonstrated relationships between the dysfunction of circadian clocks and the development of metabolic abnormalities, but the chicken-and-egg question remains unresolved. To address this issue, we investigated the cause-effect relationship in obese, diabetic ob/ob mice. Compared with control C57BL/6J mice, the daily mRNA expression profiles of the clock and clock-controlled genes Clock, Bmal1, Cry1, Per1, Per2, and Dbp were substantially dampened in the liver and adipose tissue, but not the hypothalamic suprachiasmatic nucleus, of 10-wk-old ob/ob mice. Four-week feeding of a low-calorie diet and administration of leptin over a 7-d period attenuated, to a significant and comparable extent, the observed metabolic abnormalities (obesity, hyperglycemia, hyperinsulinemia, and hypercholesterolemia) in the ob/ob mice. However, only leptin treatment improved the impaired peripheral clocks. In addition, clock function, assessed by measuring levels of Per1, Per2, and Dbp mRNA at around peak times, was also reduced in the peripheral tissues of 3-wk-old ob/ob mice without any overt metabolic abnormalities. Collectively these results indicate that the impairment of peripheral clocks in ob/ob mice does not result from metabolic abnormalities but may instead be at least partially caused by leptin deficiency itself. Further studies are needed to clarify how leptin deficiency affects peripheral clocks.

4. Shedding light on the clock

2017 ◽  
pp. 45-61
Author(s):  
Russell G. Foster ◽  
Leon Kreitzman
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
Physical Exercise ◽  
Circadian Clock ◽  
Suprachiasmatic Nucleus ◽  
Human Body ◽  
Circadian Clocks ◽  
Autonomic Nervous ◽  
Over Time ◽  
Daily Patterns

Most circadian clocks make use of a sun-based mechanism as the primary entraining signal to lock the internal day to the astronomical day. For nearly four billion years, dawn and dusk has been the main zeitgeber that allows entrainment. Circadian clocks are not exactly 24 hours. So to prevent daily patterns of activity and rest from freerunning over time, light can reset the clock. ‘Shedding light on the clock’ explains that the main circadian clock has been located in the suprachiasmatic nucleus in the hypothalamus. This also regulates the activity of the autonomic nervous system, but there are clocks in virtually every cell in the human body. Other zeitgebers include food, physical exercise, and temperature.

scholarly journals Modeling the Seasonal Adaptation of Circadian Clocks by Changes in the Network Structure of the Suprachiasmatic Nucleus

2012 ◽  
Vol 8 (9) ◽  
pp. e1002697 ◽  
Author(s):  
Christian Bodenstein ◽  
Marko Gosak ◽  
Stefan Schuster ◽  
Marko Marhl ◽  
Matjaž Perc
Keyword(s):  
Suprachiasmatic Nucleus ◽  
Network Structure ◽  
Circadian Clocks ◽  
Seasonal Adaptation

Invited Review: A neural clockwork for encoding circadian time

2002 ◽  
Vol 92 (1) ◽  
pp. 401-408 ◽  
Author(s):  
Erik D. Herzog ◽  
William J. Schwartz
Keyword(s):  
Nervous System ◽  
Single Cell ◽  
Suprachiasmatic Nucleus ◽  
Biological Rhythms ◽  
Anterior Hypothalamus ◽  
Circadian Clocks ◽  
Circadian Pacemaker ◽  
Environmental Light ◽  
Circadian Time ◽  
Oscillatory Mechanism

10.1152/japplphysiol.00836.2001.—Many daily biological rhythms are governed by an innate timekeeping mechanism or clock. Endogenous, temperature-compensated circadian clocks have been localized to discrete sites within the nervous systems of a number of organisms. In mammals, the master circadian pacemaker is the bilaterally paired suprachiasmatic nucleus (SCN) in the anterior hypothalamus. The SCN is composed of multiple single cell oscillators that must synchronize to each other and the environmental light schedule. Other tissues, including those outside the nervous system, have also been shown to express autonomous circadian periodicities. This review examines 1) how intracellular regulatory molecules function in the oscillatory mechanism and in its entrainment to environmental cycles; 2) how individual SCN cells interact to create an integrated tissue pacemaker with coherent metabolic, electrical, and secretory rhythms; and 3) how such clock outputs are converted into temporal programs for the whole organism.

scholarly journals Beyond the suprachiasmatic nucleus: Other circadian clocks in the brain

2009 ◽  
Vol 2 (6) ◽  
pp. 520-522 ◽  
Author(s):  
Jennifer A. Mohawk ◽  
Michael Menaker
Keyword(s):  
Suprachiasmatic Nucleus ◽  
Circadian Clocks ◽  
The Brain

scholarly journals Circadian Chimeric Mice Reveal an Interplay Between the Suprachiasmatic Nucleus and Local Brain Clocks in the Control of Sleep and Memory

2021 ◽  
Vol 15 ◽  
Author(s):  
Elizabeth Susan Maywood ◽  
Johanna Elizabeth Chesham ◽  
Raphaelle Winsky-Sommerer ◽  
Nicola Jane Smyllie ◽  
Michael Harvey Hastings
Keyword(s):  
Suprachiasmatic Nucleus ◽  
Ex Vivo ◽  
Circadian Clocks ◽  
Chimeric Mice ◽  
Sleep Regulation ◽  
Circadian Control ◽  
A Cell ◽  
The Brain ◽  
Local Brain

Sleep is regulated by circadian and homeostatic processes. Whereas the suprachiasmatic nucleus (SCN) is viewed as the principal mediator of circadian control, the contributions of sub-ordinate local circadian clocks distributed across the brain are unknown. To test whether the SCN and local brain clocks interact to regulate sleep, we used intersectional genetics to create temporally chimeric CK1ε Tau mice, in which dopamine 1a receptor (Drd1a)-expressing cells, a powerful pacemaking sub-population of the SCN, had a cell-autonomous circadian period of 24 h whereas the rest of the SCN and the brain had intrinsic periods of 20 h. We compared these mice with non-chimeric 24 h wild-types (WT) and 20 h CK1ε Tau mutants. The periods of the SCN ex vivo and the in vivo circadian behavior of chimeric mice were 24 h, as with WT, whereas other tissues in the chimeras had ex vivo periods of 20 h, as did all tissues from Tau mice. Nevertheless, the chimeric SCN imposed its 24 h period on the circadian patterning of sleep. When compared to 24 h WT and 20 h Tau mice, however, the sleep/wake cycle of chimeric mice under free-running conditions was disrupted, with more fragmented sleep and an increased number of short NREMS and REMS episodes. Even though the chimeras could entrain to 20 h light:dark cycles, the onset of activity and wakefulness was delayed, suggesting that SCN Drd1a-Cre cells regulate the sleep/wake transition. Chimeric mice also displayed a blunted homeostatic response to 6 h sleep deprivation (SD) with an impaired ability to recover lost sleep. Furthermore, sleep-dependent memory was compromised in chimeras, which performed significantly worse than 24 h WT and 20 h Tau mice. These results demonstrate a central role for the circadian clocks of SCN Drd1a cells in circadian sleep regulation, but they also indicate a role for extra-SCN clocks. In circumstances where the SCN and sub-ordinate local clocks are temporally mis-aligned, the SCN can maintain overall circadian control, but sleep consolidation and recovery from SD are compromised. The importance of temporal alignment between SCN and extra-SCN clocks for maintaining vigilance state, restorative sleep and memory may have relevance to circadian misalignment in humans, with environmental (e.g., shift work) causes.

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