scholarly journals Cold-inducible RNA-binding protein (CIRBP) adjusts clock-gene expression and REM-sleep recovery following sleep deprivation

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Marieke MB Hoekstra ◽  
Yann Emmenegger ◽  
Jeffrey Hubbard ◽  
Paul Franken
Keyword(s):  
Gene Expression ◽  
Sleep Deprivation ◽  
Rem Sleep ◽  
Clock Gene ◽  
Rna Binding ◽  
High Amplitude ◽  
Knock Out ◽  
Clock Gene Expression ◽  
Sleep Homeostasis

Sleep depriving mice affects clock-gene expression, suggesting that these genes contribute to sleep homeostasis. The mechanisms linking extended wakefulness to clock-gene expression are, however, not well understood. We propose CIRBP to play a role because its rhythmic expression is i) sleep-wake driven and ii) necessary for high-amplitude clock-gene expression in vitro. We therefore expect Cirbp knock-out (KO) mice to exhibit attenuated sleep-deprivation-induced changes in clock-gene expression, and consequently to differ in their sleep homeostatic regulation. Lack of CIRBP indeed blunted the sleep-deprivation incurred changes in cortical expression of Nr1d1, whereas it amplified the changes in Per2 and Clock. Concerning sleep homeostasis, KO mice accrued only half the extra REM sleep wild-type (WT) littermates obtained during recovery. Unexpectedly, KO mice were more active during lights-off which was accompanied with faster theta oscillations compared to WT mice. Thus, CIRBP adjusts cortical clock-gene expression after sleep deprivation and expedites REM-sleep recovery.

scholarly journals Cold-Inducible RNA-binding protein (CIRBP) adjusts clock gene expression and REM sleep recovery following sleep deprivation

2018 ◽  
Author(s):  
Marieke MB Hoekstra ◽  
Yann Emmenegger ◽  
Paul Franken
Keyword(s):  
Gene Expression ◽  
Sleep Deprivation ◽  
Rem Sleep ◽  
Clock Gene ◽  
Rna Binding ◽  
High Amplitude ◽  
Knock Out ◽  
Clock Gene Expression ◽  
Sleep Homeostasis

AbstractSleep depriving mice affects clock gene expression, suggesting that these genes partake in sleep homeostasis. The mechanisms linking wakefulness to clock gene expression are, however, not well understood. We propose CIRBP because its rhythmic expression is i) sleep-wake driven and ii) necessary for high-amplitude clock gene expression in vitro. We therefore expect Cirbp knock-out (KO) mice to exhibit attenuated sleep-deprivation (SD) induced changes in clock gene expression, and consequently to differ in their sleep homeostatic regulation. Lack of CIRBP indeed blunted the SD-incurred changes in cortical expression of the clock gene Rev-erbα whereas it amplified the changes in Per2 and Clock. Concerning sleep homeostasis, KO mice accrued only half the extra REM sleep wild-type (WT) littermates obtained during recovery. Unexpectedly, KO mice were more active during lights-off which was accompanied by an acceleration of theta oscillations. Thus, CIRBP adjusts cortical clock gene expression after SD and expedites REM sleep recovery.

scholarly journals Simultaneous Monitoring of Behavior & Peripheral Clocks in Drosophila Reveals Unstructured Sleep in an Alzheimer's Model

2015 ◽  
Author(s):  
Eleonora Khabirova ◽  
Ko-Fan Chen ◽  
John S O'Neill ◽  
Damian C Crowther
Keyword(s):  
Gene Expression ◽  
Clock Gene ◽  
Biological Clock ◽  
Model Organisms ◽  
Clock Gene Expression ◽  
Biological Phenomena ◽  
Model Of Alzheimer’S Disease ◽  
Sleep Homeostasis ◽  
Regulatory Machinery ◽  
Activity Cycles

Sleep and circadian rhythms are ancient, related biological phenomena controlled by distinct neuronal circuits, whose appropriate regulation is critical for health. Whereas the regulatory machinery underlying sleep homeostasis is ill-defined, the biological clock mechanism is better understood: from cell-intrinsic feedback loops of ‘clock gene’ expression to circuits that facilitate rhythmic behavior. Age- and neurodegeneration related deterioration in sleep/wake timing was first described in humans decades ago, but has only recently been recapitulated in model organisms. In order to delineate the causal relationships between aging, sleep, neuronal function and the molecular clockwork, we have developed FLYGLOW, a broadly applicable bioluminescence-based system which allows rest/activity cycles, sleep consolidation and molecular clock gene expression to be quantified simultaneously in dozens of individual flies over many days/weeks. We show that FLYGLOW outperforms existing methods, and demonstrate the utility of the multiparameter correlational analyses within and between flies that it enables. We go on to show unambiguously that peripheral cellular rhythms can free-run independently of the central pacemakers that drive behavioural cycles. Finally, using a fly model of Alzheimer’s disease (AD) we observe a profound disorganization of sleep and activity cycles, that phenocopies the human disease.

scholarly journals The Circadian Oscillator of the Cerebellum: Triiodothyronine Regulates Clock Gene Expression in Granule Cells in vitro and in the Cerebellum of Neonatal Rats in vivo

2021 ◽  
Vol 12 ◽  
Author(s):  
Tenna Bering ◽  
Henrik Hertz ◽  
Martin Fredensborg Rath
Keyword(s):  
Gene Expression ◽  
Clock Gene ◽  
Granule Cells ◽  
Clock Genes ◽  
Circadian Oscillator ◽  
Neonatal Rats ◽  
Clock Gene Expression ◽  
Mixed Gender

The central circadian clock resides in the suprachiasmatic nucleus (SCN) of the hypothalamus, but an SCN-dependent molecular circadian oscillator is present in the cerebellar cortex. Recent findings suggest that circadian release of corticosterone is capable of driving the circadian oscillator of the rat cerebellum. To determine if additional neuroendocrine signals act to shape cerebellar clock gene expression, we here tested the role of the thyroid hormone triiodothyronine (T3) in regulation of the cerebellar circadian oscillator. In cultured cerebellar granule cells from mixed-gender neonatal rats, T3 treatment affected transcript levels of the clock genes Per2, Arntl, Nr1d1, and Dbp, suggesting that T3 acts directly on granule cells to control the circadian oscillator. We then used two different in vivo protocols to test the role of T3 in adult female rats: Firstly, a single injection of T3 did not influence clock gene expression in the cerebellum. Secondly, we established a surgical rat model combining SCN lesion with a programmable micropump infusing circadian physiological levels of T3; however, rhythmic infusion of T3 did not reestablish differential clock gene expression between day and night in SCN lesioned rats. To test if the effects of T3 observed in vitro were related to the developmental stage, acute injections of T3 were performed in mixed-gender neonatal rats in vivo; this procedure significantly affected cerebellar expression of the clock genes Per1, Per2, Nr1d1, and Dbp. Developmental comparisons showed rhythmic expression of all clock genes analyzed in the cerebellum of adult rats only, whereas T3 responsiveness was limited to neonatal animals. Thus, T3 shapes cerebellar clock gene profiles in early postnatal stages, but it does not represent a systemic circadian regulatory mechanism linking the SCN to the cerebellum throughout life.

scholarly journals Disrupted Sleep Homeostasis and Altered Expressions of Clock Genes in Rats with Chronic Lead Exposure

Toxics ◽  
2021 ◽  
Vol 9 (9) ◽  
pp. 217
Author(s):  
Chung-Yao Hsu ◽  
Yao-Chung Chuang ◽  
Fang-Chia Chang ◽  
Hung-Yi Chuang ◽  
Terry Ting-Yu Chiou ◽  
...  
Keyword(s):  
Gene Expression ◽  
Lead Exposure ◽  
Clock Gene ◽  
Slow Wave Sleep ◽  
Clock Genes ◽  
Negative Impact ◽  
Dark Period ◽  
Clock Gene Expression ◽  
Sleep Homeostasis ◽  
Chronic Lead Exposure

Sleep disturbance is one of the neurobehavioral complications of lead neurotoxicity. The present study evaluated the impacts of chronic lead exposure on alteration of the sleep–wake cycle in association with changes of clock gene expression in the hypothalamus. Sprague–Dawley rats with chronic lead exposure consumed drinking water that contained 250 ppm of lead acetate for five weeks. Electroencephalography and electromyography were recorded for scoring the architecture of the sleep–wake cycle in animals. At six Zeitgeber time (ZT) points (ZT2, ZT6, ZT10, ZT14, ZT18, and ZT22), three clock genes, including rPer1, rPer2, and rBmal1b, were analyzed. The rats with chronic lead exposure showed decreased slow wave sleep and increased wakefulness in the whole light period (ZT1 to ZT12) and the early dark period (ZT13 to ZT15) that was followed with a rebound of rapid-eye-movement sleep at the end of the dark period (ZT22 to ZT24). The disturbance of the sleep–wake cycle was associated with changes in clock gene expression that was characterized by the upregulation of rPer1 and rPer2 and the feedback repression of rBmal1b. We concluded that chronic lead exposure has a negative impact on the sleep–wake cycle in rats that predominantly disrupts sleep homeostasis. The disruption of sleep homeostasis was associated with a toxic effect of lead on the clock gene expression in the hypothalamus.

scholarly journals Effect of sleep deprivation on rhythms of clock gene expression and melatonin in humans

2013 ◽  
Vol 30 (7) ◽  
pp. 901-909 ◽  
Author(s):  
Katrin Ackermann ◽  
Rosina Plomp ◽  
Oscar Lao ◽  
Benita Middleton ◽  
Victoria L. Revell ◽  
...  
Keyword(s):  
Gene Expression ◽  
Sleep Deprivation ◽  
Clock Gene ◽  
Clock Gene Expression
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