A Circadian Rhythm in the Expression of PERIOD2 Protein Reveals a Novel SCN-Controlled Oscillator in the Oval Nucleus of the Bed Nucleus of the Stria Terminalis

Amir, Shimon; Lamont, Elaine Waddington; Robinson, Barry; Stewart, Jane

doi:10.1523/jneurosci.4488-03.2004

Cited by 146 publications

(188 citation statements)

References 85 publications

(112 reference statements)

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“…These are core clock genes that serve to regulate the near-24 -hour regulation of clock-controlled gene transcription and ultimately manifest circadian rhythmicity at the physiological level. Both the BNST and the cingulate cortex have previously been shown to express rhythmic clock genes (10,53). Similar peak times for PER1 and PER2 in control subjects in the active phase were reported, whereas BMAL1 was shown to peak in the night (52).…”

Section: Clock Gene Cycles In Adsupporting

confidence: 69%

The Circadian System in Alzheimer’s Disease: Disturbances, Mechanisms, and Opportunities

Coogan

Schutová

Husung

et al. 2013

Biological Psychiatry

146

131

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Alzheimer's disease (AD) is a devastating neurodegenerative condition associated with severe cognitive and behavioral impairments. Circadian rhythms are recurring cycles that display periods of approximately 24 hours and are driven by an endogenous circadian timekeeping system centered on the suprachiasmatic nucleus of the hypothalamus. We review the compelling evidence that circadian rhythms are significantly disturbed in AD and that such disturbance is of significant clinical importance in terms of behavioral symptoms. We also detail findings from neuropathological studies of brain areas associated with the circadian system in postmortem studies, the use of animal models of AD in the investigation of circadian processes, and the evidence that chronotherapeutic approaches aimed at bolstering weakened circadian rhythms in AD produce beneficial outcomes. We argue that further investigation in such areas is warranted and highlight areas for future research that might prove fruitful in ultimately providing new treatment options for this most serious and intractable of conditions.

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Section: Clock Gene Cycles In Adsupporting

confidence: 69%

The Circadian System in Alzheimer’s Disease: Disturbances, Mechanisms, and Opportunities

Coogan

Schutová

Husung

et al. 2013

Biological Psychiatry

146

131

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“…For instance, rhythmic expression of Per1 and Per2 mRNA is observed in forebrain structures such as olfactory bulbs, piriform and cerebral cortices, hippocampus, paraventricular and arcuate hypothalamic nuclei (Asai et al, 2001;Wakamatsu et al, 2001;Abe et al, 2002;Granados-Fuentes et al, 2004). PER2 expression has also been reported in limbic structures, such as amygdala and bed nucleus of the stria terminalis (Amir et al, 2004;Lamont et al, 2005). Except for the SCN in which the rhythm of PERs follows the mRNA expression by 4-6 h (Field et al, 2000;Mendoza et al, 2007), little is known about the exact timing of both PER1 and PER2 oscillations in forebrain structures.…”

Section: Introductionmentioning

confidence: 99%

Forebrain oscillators ticking with different clock hands

Feillet

Mendoza

Albrecht

et al. 2008

Molecular and Cellular Neuroscience

133

113

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Clock proteins like PER1 and PER2 are expressed in the brain, but little is known about their functionality outside the main suprachiasmatic clock. Here we show that PER1 and PER2 were neither uniformly present nor identically phased in forebrain structures of mice fed ad libitum. Altered expression of the clock gene Cry1 was observed in respective Per1 or Per2 mutants. In response to hypocaloric feeding, PERs timing was not markedly affected in few forebrain structures (hippocampus). In most other forebrain oscillators, including those expressing only PER1 (e.g., dorsomedial hypothalamus), PER2 (e.g., paraventricular hypothalamus) or both (e.g., paraventricular thalamus), PER1 was up-regulated and PER2 largely phase-advanced. Cry1 expression was selectively modified in the forebrain of Per mutants challenged with hypocaloric feeding. Our results suggest that there is not one single cerebral clock, but a system of multiple brain oscillators ticking with different clock hands and differentially sensitive to nutritional cues.

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“…The interaction of glucocorticoid and circadian clock control of cell proliferation may not be limited to one single mechanism, given the diverse effects of glucocorticoids on cell proliferation in different tissues. As mentioned above, a similar situation exists for the contribution of glucocorticoids to circadian clock gene cycling in different tissues: While circadian per2 expression in some regions of the brain depends on glucocorticoids [111,112], this is not the case in other brain regions [112] or the liver [44,114]. Clearly, similar tissue specific differences might also be at work in the control of circadian cell cycle rhythms by glucocorticoids, with rhythmic glucocorticoid presence required in some tissues and tonic levels being sufficient in others.…”

Section: Glucocorticoids and Rhythms Of Cell Proliferationmentioning

confidence: 71%

“…However, mice lacking the glucocorticoid receptor in the liver still exhibit phases of clock gene expression identical to those of their wild type siblings, arguing against a strict requirement for glucocorticoids in liver clock entrainment [44]. Nevertheless, glucocorticoids do appear to be required for normal circadian expression of per2 in some areas of the brain, since cycling M a n u s c r i p t expression of this gene is abolished in adrenalectomised animals (animals in which the adrenal gland has been removed) [111,112]. Interestingly, the per2 rhythms can resume when diurnal changes in corticosterone are restored in adrenalectomised animals by delivering corticosterone with the drinking water.…”

Section: Glucocorticoids Talk Back To the Clock?mentioning

confidence: 99%

Glucocorticoids and circadian clock control of cell proliferation: At the interface between three dynamic systems

Dickmeis

Foulkes

2011

Molecular and Cellular Endocrinology

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The circadian clock, an endogenous timekeeper that regulates daily rhythms of physiology, also influences the dynamic release of glucocorticoids. The release of glucocorticoids is characteristically pulsatile and is further modulated in a circadian fashion. A circadian pacemaker in the brain regulates daily rhythms of hypothalamicpituitary-adrenal axis and autonomic nervous system activity that both influence glucocorticoid release from the adrenal gland. This systemic regulation interacts with rhythms in the adrenal gland itself that are driven by its own circadian clock. One function of glucocorticoids is the regulation of cell proliferation. Depending on the tissue, this can involve both negative and positive regulation of a variety of processes, including cell differentiation and cell death. Cell proliferation is also under circadian control, and recent evidence suggests that this regulation may involve glucocorticoid signalling. Here, we review the dynamic processes participating in the interplay between the circadian clock, glucocorticoids and cell proliferation, and we discuss the potential implications for therapy.

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A Circadian Rhythm in the Expression of PERIOD2 Protein Reveals a Novel SCN-Controlled Oscillator in the Oval Nucleus of the Bed Nucleus of the Stria Terminalis

Cited by 146 publications

References 85 publications

The Circadian System in Alzheimer’s Disease: Disturbances, Mechanisms, and Opportunities

The Circadian System in Alzheimer’s Disease: Disturbances, Mechanisms, and Opportunities

Forebrain oscillators ticking with different clock hands

Glucocorticoids and circadian clock control of cell proliferation: At the interface between three dynamic systems

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