scholarly journals Circadian rhythms of clock gene expression in the cerebellum of serotonin-deficient Pet-1 knockout mice

2016 ◽  
Vol 1630 ◽  
pp. 10-17 ◽  
Author(s):  
Erin V. Paulus ◽  
Eric M. Mintz
2019 ◽  
Author(s):  
M Schlichting ◽  
MM Diaz ◽  
J Xin ◽  
M Rosbash

AbstractAnimal circadian rhythms persist in constant darkness and are driven by intracellular transcription-translation feedback loops. Although these cellular oscillators communicate, isolated mammalian cellular clocks continue to tick away in darkness without intercellular communication. To investigate these issues in Drosophila, we assayed behavior as well as molecular rhythms within individual brain clock neurons while blocking communication within the ca. 150 neuron clock network. We also generated CRISPR-mediated neuron-specific circadian clock knockouts. The results point to two key clock neuron groups: loss of the clock within both regions but neither one alone has a strong behavioral phenotype in darkness; communication between these regions also contributes to circadian period determination. Under these dark conditions, the clock within one region persists without network communication. The clock within the famous PDF-expressing s-LNv neurons however was strongly dependent on network communication, likely because clock gene expression within these vulnerable sLNvs depends on neuronal firing or light.


2020 ◽  
Vol 133 (21) ◽  
pp. 2635-2637
Author(s):  
Xian-Xian Zhang ◽  
Xiu-Ying Cai ◽  
Hong-Ru Zhao ◽  
Hui Wang ◽  
Da-Peng Wang ◽  
...  

2011 ◽  
Vol 26 (1) ◽  
pp. 78-81 ◽  
Author(s):  
Brian P. Grone ◽  
Doris Chang ◽  
Patrice Bourgin ◽  
Vinh Cao ◽  
Russell D. Fernald ◽  
...  

F1000Research ◽  
2016 ◽  
Vol 5 ◽  
pp. 2062 ◽  
Author(s):  
Michael Verwey ◽  
Sabine Dhir ◽  
Shimon Amir

Circadian clock proteins form an autoregulatory feedback loop that is central to the endogenous generation and transmission of daily rhythms in behavior and physiology. Increasingly, circadian rhythms in clock gene expression are being reported in diverse tissues and brain regions that lie outside of the suprachiasmatic nucleus (SCN), the master circadian clock in mammals. For many of these extra-SCN rhythms, however, the region-specific implications are still emerging. In order to gain important insights into the potential behavioral, physiological, and psychological relevance of these daily oscillations, researchers have begun to focus on describing the neurochemical, hormonal, metabolic, and epigenetic contributions to the regulation of these rhythms. This review will highlight important sites and sources of circadian control within dopaminergic and striatal circuitries of the brain and will discuss potential implications for psychopathology and disease. For example, rhythms in clock gene expression in the dorsal striatum are sensitive to changes in dopamine release, which has potential implications for Parkinson’s disease and drug addiction. Rhythms in the ventral striatum and limbic forebrain are sensitive to psychological and physical stressors, which may have implications for major depressive disorder. Collectively, a rich circadian tapestry has emerged that forces us to expand traditional views and to reconsider the psychopathological, behavioral, and physiological importance of these region-specific rhythms in brain areas that are not immediately linked with the regulation of circadian rhythms.


2012 ◽  
Vol 236 (2) ◽  
pp. 249-258 ◽  
Author(s):  
Marilyn J. Duncan ◽  
J. Tyler Smith ◽  
Kathleen M. Franklin ◽  
Tina L. Beckett ◽  
M. Paul Murphy ◽  
...  

2007 ◽  
Vol 293 (4) ◽  
pp. R1528-R1537 ◽  
Author(s):  
David J. Kennaway ◽  
Julie A. Owens ◽  
Athena Voultsios ◽  
Michael J. Boden ◽  
Tamara J. Varcoe

The role of peripheral vs. central circadian rhythms and Clock in the maintenance of metabolic homeostasis and with aging was examined by using ClockΔ19 +MEL mice. These have preserved suprachiasmatic nucleus and pineal gland rhythmicity but arrhythmic Clock gene expression in the liver and skeletal muscle. ClockΔ19 +MEL mice showed fasting hypoglycemia in young-adult males, fasting hyperglycemia in older females, and substantially impaired glucose tolerance overall. ClockΔ19 +MEL mice had substantially reduced plasma insulin and plasma insulin/glucose nocturnally in males and during a glucose tolerance test in females, suggesting impaired insulin secretion. ClockΔ19 +MEL mice had reduced hepatic expression and loss of rhythmicity of gck, pfkfb3, and pepck mRNA, which is likely to impair glycolysis and gluconeogenesis. ClockΔ19 +MEL mice also had reduced glut4 mRNA in skeletal muscle, and this may contribute to poor glucose tolerance. Whole body insulin tolerance was enhanced in ClockΔ19 +MEL mice, however, suggesting enhanced insulin sensitivity. These responses occurred although the ClockΔ19 mutation did not cause obesity and reduced plasma free fatty acids while increasing plasma adiponectin. These studies on clock-gene disruption in peripheral tissues and metabolic homeostasis provide compelling evidence of a relationship between circadian rhythms and the glucose/insulin and adipoinsular axes. It is, however, premature to declare that clock-gene disruption causes the full metabolic syndrome.


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