Light affects behavioral despair involving the clock gene Period 1

Light at night has strong effects on physiology and behavior of mammals. It affects mood in humans, which is exploited as light therapy, and has been shown to reset the circadian clock in the suprachiasmatic nuclei (SCN). This resetting is paramount to align physiological and biochemical timing to the environmental light-dark cycle. Here we provide evidence that light at zeitgeber time (ZT) 22 affects mood-related behaviors also in mice by activating the clock gene Period1 (Per1) in the lateral habenula (LHb), a brain region known to modulate mood-related behaviors. We show that complete deletion of Per1 in mice led to depressive-like behavior and loss of the beneficial effects of light on this behavior. In contrast, specific deletion of Per1 in the region of the LHb did not affect mood-related behavior, but suppressed the beneficial effects of light. RNA sequence analysis in the mesolimbic dopaminergic system revealed profound changes of gene expression after a light pulse at ZT22. In the nucleus accumbens (NAc), sensory perception of smell and G-protein coupled receptor signaling were affected the most. Interestingly, most of these genes were not affected in Per1 knock-out animals, indicating that induction of Per1 by light serves as a filter for light-mediated gene expression in the brain. Taken together we show that light affects mood-related behavior in mice at least in part via induction of Per1 in the LHb with consequences on mood-related behavior and signaling mechanisms in the mesolimbic dopaminergic system.

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Light affects behavioral despair involving the clock gene Period 1

10.1101/2020.05.07.082156 ◽

2020 ◽

Author(s):

Iwona Olejniczak ◽

Jürgen A. Ripperger ◽

Federica Sandrelli ◽

Anna Schnell ◽

Laureen Mansencal-Strittmatter ◽

...

Keyword(s):

Brain Region ◽

Clock Gene ◽

Dopaminergic System ◽

Light Therapy ◽

Suprachiasmatic Nuclei ◽

Lateral Habenula ◽

Knock Out ◽

Environmental Light ◽

And Behavior ◽

G Protein Coupled

AbstractLight at night has strong effects on physiology and behavior of mammals. It affects mood in humans, which is exploited as light therapy, and has been shown to reset the circadian clock in the suprachiasmatic nuclei (SCN). This resetting is paramount to align physiological and biochemical timing to the environmental light-dark cycle. Here we provide evidence that light affects mood-related behaviors also in mice by activating the clock gene Period1 (Per1) in the lateral habenula (LHb), a brain region known to modulate mood-related behaviors. A light pulse given at ZT22 to wild type mice caused profound changes of gene expression in the mesolimbic dopaminergic system including the nucleus accumbens (NAc). Sensory perception of smell and G-protein coupled receptor signaling was affected the most in this brain region. Interestingly, most of these genes were not affected in Per1 knock-out animals, indicating that induction of Per1 by light serves as a filter for light-mediated gene induction in the brain. Taken together we show that light affects mood-related behavior in mice at least in part via induction of Per1 in the LHb with consequences on signaling mechanisms in the mesolimbic dopaminergic system.

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Transmembrane Signaling in the Brain by Serotonin, A Key Regulator of Physiology and Emotion

Bioscience Reports ◽

10.1007/s10540-005-2896-3 ◽

2005 ◽

Vol 25 (5-6) ◽

pp. 363-385 ◽

Cited By ~ 40

Author(s):

Tatyana Adayev ◽

Buddima Ranasinghe ◽

Probal Banerjee

Keyword(s):

Gene Expression ◽

Immune Cells ◽

Functional Role ◽

Living Organism ◽

Covalent Modification ◽

G Protein Coupled Receptors ◽

And Behavior ◽

G Protein Coupled ◽

Compare And Contrast ◽

The Brain

Serotonin (5-HT) is an ancient chemical that plays a crucial functional role in almost every living organism. It regulates platelet aggregation, activation of immune cells, and contraction of stomach and intestinal muscles. In addition, serotonin acts as a neurotransmitter in the brain and the peripheral nervous system. These activities are initiated by the binding of serotonin to 15 or more receptors that are pharmacologically classified into seven groups, 5-HT1 through 5-HT7. Each group is further divided into subgroups of receptors that are homologous but are encoded by discrete genes. With the exception of the 5-HT3 receptor-a cation channel—all of the others are G protein-coupled receptors that potentially activate or inhibit a large number of biochemical cascades. This review will endeavor to compare and contrast such signaling pathways with special attention to their tissue-specific occurrence, their possible role in immediate effects on covalent modification of other proteins, and relatively slower effects on gene expression, physiology and behavior.

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Artificial Light at Night Influences Clock-Gene Expression, Activity, and Fecundity in the Mosquito Culex pipiens f. molestus

Sustainability ◽

10.3390/su11226220 ◽

2019 ◽

Vol 11 (22) ◽

pp. 6220 ◽

Cited By ~ 2

Author(s):

Honnen ◽

Kypke ◽

Hölker ◽

Monaghan

Keyword(s):

Gene Expression ◽

Culex Pipiens ◽

Clock Gene ◽

Clock Cycle ◽

Diel Activity ◽

Artificial Light ◽

Light At Night ◽

Clock Gene Expression ◽

Expression Activity ◽

And Behavior

Light is an important environmental cue, and exposure to artificial light at night (ALAN) may disrupt organismal physiology and behavior. We investigated whether ALAN led to changes in clock-gene expression, diel activity patterns, and fecundity in laboratory populations of the mosquito Culex pipiens f. molestus (Diptera, Culicidae), a species that occurs in urban areas and is thus regularly exposed to ALAN. Populations were kept under 16hours (h):8h light:dark cycles or were subjected to an additional 3.5 h of light (100–300 lx) in the evenings. ALAN induced significant changes in expression in all genes studied, either alone (period) or as an interaction with time (timeless, cryptochrome2, Clock, cycle). Changes were sex-specific: period was down-regulated in both sexes, cycle was up-regulated in females, and Clock was down-regulated in males. ALAN-exposed mosquitoes were less active during the extra-light phase, but exposed females were more active later in the night. ALAN-exposed females also produced smaller and fewer eggs. Our findings indicate a sex-specific impact of ALAN on the physiology and behavior of Culex pipiens f. molestus and that changes in clock-gene expression, activity, and fecundity may be linked.

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Circadian disruption alters mouse lung clock gene expression and lung mechanics

Journal of Applied Physiology ◽

10.1152/japplphysiol.00244.2012 ◽

2012 ◽

Vol 113 (3) ◽

pp. 385-392 ◽

Cited By ~ 28

Author(s):

Hélène Hadden ◽

Steven J. Soldin ◽

Donald Massaro

Keyword(s):

Gene Expression ◽

Clock Gene ◽

Clock Genes ◽

Circadian Disruption ◽

Lung Mechanics ◽

Mouse Lung ◽

Clock Gene Expression ◽

Light Regimen ◽

And Behavior ◽

And Control

Most aspects of human physiology and behavior exhibit 24-h rhythms driven by a master circadian clock in the brain, which synchronizes peripheral clocks. Lung function and ventilation are subject to circadian regulation and exhibit circadian oscillations. Sleep disruption, which causes circadian disruption, is common in those with chronic lung disease, and in the general population; however, little is known about the effect on the lung of circadian disruption. We tested the hypothesis circadian disruption alters expression of clock genes in the lung and that this is associated with altered lung mechanics. Female and male mice were maintained on a 12:12-h light/dark cycle (control) or exposed for 4 wk to a shifting light regimen mimicking chronic jet lag (CJL). Airway resistance (Rn), tissue damping (G), and tissue elastance (H) did not differ between control and CJL females. Rn at positive end-expiratory pressure (PEEP) of 2 and 3 cmH2O was lower in CJL males compared with controls. G, H, and G/H did not differ between CJL and control males. Among CJL females, expression of clock genes, Bmal1 and Rev-erb alpha, was decreased; expression of their repressors, Per2 and Cry 2, was increased. Among CJL males, expression of Clock was decreased; Per 2 and Rev-erb alpha expression was increased. We conclude circadian disruption alters lung mechanics and clock gene expression and does so in a sexually dimorphic manner.

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

10.1101/476911 ◽

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.

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

eLife ◽

10.7554/elife.43400 ◽

2019 ◽

Vol 8 ◽

Cited By ~ 18

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.

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