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
2008 ◽  
Vol 6 (2) ◽  
pp. 84-90 ◽  
Author(s):  
Sato HONMA ◽  
Natsuko INAGAKI ◽  
Daisuke ONO ◽  
Tomoko YOSHIKAWA ◽  
Satoko HASHIMOTO ◽  
...  

Endocrinology ◽  
2011 ◽  
Vol 152 (4) ◽  
pp. 1347-1354 ◽  
Author(s):  
Hitoshi Ando ◽  
Masafumi Kumazaki ◽  
Yuya Motosugi ◽  
Kentarou Ushijima ◽  
Tomohiro Maekawa ◽  
...  

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.


Author(s):  
Russell G. Foster ◽  
Leon Kreitzman

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.


2019 ◽  
Vol 34 (5) ◽  
pp. 515-524
Author(s):  
Changgui Gu ◽  
Xiangwei Gu ◽  
Ping Wang ◽  
Henggang Ren ◽  
Tongfeng Weng ◽  
...  

In mammals, an endogenous clock located in the suprachiasmatic nucleus (SCN) of the brain regulates the circadian rhythms of physiological and behavioral activities. The SCN is composed of about 20,000 neurons that are autonomous oscillators with nonidentical intrinsic periods ranging from 22 h to 28 h. These neurons are coupled through neurotransmitters and synchronized to form a network, which produces a robust circadian rhythm of a uniform period. The neurons, which are the nodes in the network, are known to be heterogeneous in their characteristics, which is reflected in different phenotypes and different functionality. This heterogeneous nature of the nodes of the network leads to the question as to whether the structure of the SCN network is assortative or disassortative. Thus far, the disassortativity of the SCN network has not been assessed and neither have its effects on the collective behaviors of the SCN neurons. In the present study, we build a directed SCN network composed of hundreds of neurons for a single slice using the method of transfer entropy, based on the experimental data. Then, we measured the synchronization degree as well as the disassortativity coefficient of the network structure (calculated by either the out-degrees or the in-degrees of the nodes) and found that the network of the SCN is a disassortative network. Furthermore, a positive relationship is observed between the synchronization degree and disassortativity of the network, which is confirmed by simulations of our modeling. Our finding suggests that the disassortativity of the network structure plays a role in the synchronization between SCN neurons; that is, the synchronization degree increases with the increase of the disassortativity, which implies that a more heterogeneous coupling in the network of the SCN is important for proper function of the SCN.


Diabetes ◽  
2013 ◽  
Vol 62 (4) ◽  
pp. 1017-1019 ◽  
Author(s):  
J. M. Radziuk

2002 ◽  
Vol 92 (1) ◽  
pp. 401-408 ◽  
Author(s):  
Erik D. Herzog ◽  
William J. Schwartz

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.


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