Exogenous Corticosterone Induces the Expression of the Clock Protein, PERIOD2, in the Oval Nucleus of the Bed Nucleus of the Stria Terminalis and the Central Nucleus of the Amygdala of Adrenalectomized and Intact Rats

Segall, Lauren; Amir, Shimon

doi:10.1007/s12031-010-9375-4

Cited by 28 publications

(21 citation statements)

References 30 publications

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“…Corticosterone is a potent transcriptional regulator that is critical for the rhythmic expression of the clock gene per2 in the oval nucleus of the bed nucleus of the stria terminalis and central nucleus of the amygdala [28], [59]–[61]. The daily CORT rhythm regulates μ-opioid receptor expression in the brainstem [29] and drives tryptophan hydroxylase-2 expression in serotonergic neurons in the dorsal and median raphe [30], [31].…”

Section: Discussionmentioning

confidence: 99%

Altered Entrainment to the Day/Night Cycle Attenuates the Daily Rise in Circulating Corticosterone in the Mouse

et al. 2014

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The suprachiasmatic nucleus (SCN) is a circadian oscillator entrained to the day/night cycle via input from the retina. Serotonin (5-HT) afferents to the SCN modulate retinal signals via activation of 5-HT1B receptors, decreasing responsiveness to light. Consequently, 5-HT1B receptor knockout (KO) mice entrain to the day/night cycle with delayed activity onsets. Since circulating corticosterone levels exhibit a robust daily rhythm peaking around activity onset, we asked whether delayed entrainment of activity onsets affects rhythmic corticosterone secretion. Wheel-running activity and plasma corticosterone were monitored in mice housed under several different lighting regimens. Both duration of the light∶dark cycle (T cycle) and the duration of light within that cycle was altered. 5-HT1B KO mice that entrained to a 9.5L:13.5D (short day in a T = 23 h) cycle with activity onsets delayed more than 4 h after light offset exhibited a corticosterone rhythm in phase with activity rhythms but reduced 50% in amplitude compared to animals that initiated daily activity <4 h after light offset. Wild type mice in 8L:14D (short day in a T = 22 h) conditions with highly delayed activity onsets also exhibited a 50% reduction in peak plasma corticosterone levels. Exogenous adrenocorticotropin (ACTH) stimulation in animals exhibiting highly delayed entrainment suggested that the endogenous rhythm of adrenal responsiveness to ACTH remained aligned with SCN-driven behavioral activity. Circadian clock gene expression in the adrenal cortex of these same animals suggested that the adrenal circadian clock was also aligned with SCN-driven behavior. Under T cycles <24 h, altered circadian entrainment to short day (winter-like) conditions, manifest as long delays in activity onset after light offset, severely reduces the amplitude of the diurnal rhythm of plasma corticosterone. Such a pronounced reduction in the glucocorticoid rhythm may alter rhythmic gene expression in the central nervous system and in peripheral organs contributing to an array of potential pathophysiologies.

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Section: Discussionmentioning

confidence: 99%

Altered Entrainment to the Day/Night Cycle Attenuates the Daily Rise in Circulating Corticosterone in the Mouse

et al. 2014

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“…Rats were allowed free access to food and water at all times. During the 2-week entrainment period, ADX rats were given CORT in their drinking water to prevent disruption of normal PER rhythms as previously described [15, 16]. CORT (Sigma-Aldrich, Oakville, ON, Canada) was dissolved in 0.9% saline, at a concentration of 25 mg/l [15].…”

Section: Methodsmentioning

confidence: 99%

“…For example, it has been shown that treatment with dexamethasone, a synthetic glucocorticoid, induces circadian gene expression in cultured rat-1 fibroblasts, and can transiently alter the phase of circadian gene expression in the liver, kidneys, and heart [11, 12]. Furthermore, we have shown that depletion of endogenous glucocorticoids via adrenalectomy (ADX) or selective genetic deletion of brain glucocorticoid receptors (GR), blunt the rhythm of expression of the clock protein, PER2 in nuclei of the central extended amygdala, the oval nucleus of the bed nucleus of the stria terminalis (BNSTov) and the lateral part of the central nucleus of the amygdala (CEAl), without affecting the rhythms of the SCN in rats [13–16]. …”

Section: Introductionmentioning

confidence: 99%

Glucocorticoids and Stress-Induced Changes in the Expression of PERIOD1 in the Rat Forebrain

et al. 2015

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The secretion of glucocorticoids in mammals is under circadian control, but glucocorticoids themselves are also implicated in modulating circadian clock gene expression. We have shown that the expression of the circadian clock protein PER1 in the forebrain is modulated by stress, and that this effect is associated with changes in plasma corticosterone levels, suggesting a possible role for glucocorticoids in the mediation of stress-induced changes in the expression of PER1 in the brain. To study this, we assessed the effects of adrenalectomy and of pretreatment with the glucocorticoid receptor antagonist, mifepristone, on the expression of PER1 in select limbic and hypothalamic regions following acute exposure to a neurogenic stressor, restraint, or a systemic stressor, 2-Deoxy-D-glucose (2DG) in rats. Acute restraint suppressed PER1 expression in the oval nucleus of the bed nucleus of the stria terminalis (BNSTov) and the central nucleus of the amygdala (CEAl), whereas 2DG increased PER1 in both regions. Both stressors increased PER1 expression in the paraventricular (PVN) and dorsomedial (DMH) nuclei of the hypothalamus, and the piriform cortex (Pi). Adrenalectomy and pretreatment with mifepristone reversed the effects of both stressors on PER1 expression in the BNSTov and CEAl, and blocked their effects in the DMH. In contrast, both treatments enhanced the effects of restraint and 2DG on PER1 levels in the PVN. Stress-induced PER1 expression in the Pi was unaffected by either treatment. PER1 expression in the suprachiasmatic nucleus, the master circadian clock, was not altered by either exposure to stress or by the glucocorticoid manipulations. Together, the results demonstrate a key role for glucocorticoid signaling in stress-induced changes in PER1 expression in the brain.

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“…A similar impact of stress on Per2 has also been demonstrated. In the mouse limbic areas, for instance, protein expression of PER2 is strictly controlled by glucocorticoids (Segall & Amir, 2010a, 2010b). Furthermore, glucocorticoid receptor (GR) function is necessary for the rhythmic expression of the clock protein PER2, because neuron-specific GR-inducible mutant mice do not display a daily rhythm of PER2 activity (Segall, Milet, Tronche, & Amir, 2009).…”

Section: Stress Affects Clock Genesmentioning

confidence: 99%

Clock genes × stress × reward interactions in alcohol and substance use disorders

Perreau-Lenz

Spanagel

2015

Alcohol

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Adverse life events and highly stressful environments have deleterious consequences for mental health. Those environmental factors can potentiate alcohol and drug abuse in vulnerable individuals carrying specific genetic risk factors, hence producing the final risk for alcohol- and substance-use disorders development. The nature of these genes remains to be fully determined, but studies indicate their direct or indirect relation to the stress hypothalamo-pituitary-adrenal (HPA) axis and/or reward systems. Over the past decade, clock genes have been revealed to be key-players in influencing acute and chronic alcohol/drug effects. In parallel, the influence of chronic stress and stressful life events in promoting alcohol and substance use and abuse has been demonstrated. Furthermore, the reciprocal interaction of clock genes with various HPA-axis components, as well as the evidence for an implication of clock genes in stress-induced alcohol abuse, have led to the idea that clock genes, and Period genes in particular, may represent key genetic factors to consider when examining gene × environment interaction in the etiology of addiction. The aim of the present review is to summarize findings linking clock genes, stress, and alcohol and substance abuse, and to propose potential underlying neurobiological mechanisms.

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Exogenous Corticosterone Induces the Expression of the Clock Protein, PERIOD2, in the Oval Nucleus of the Bed Nucleus of the Stria Terminalis and the Central Nucleus of the Amygdala of Adrenalectomized and Intact Rats

Cited by 28 publications

References 30 publications

Altered Entrainment to the Day/Night Cycle Attenuates the Daily Rise in Circulating Corticosterone in the Mouse

Altered Entrainment to the Day/Night Cycle Attenuates the Daily Rise in Circulating Corticosterone in the Mouse

Glucocorticoids and Stress-Induced Changes in the Expression of PERIOD1 in the Rat Forebrain

Clock genes × stress × reward interactions in alcohol and substance use disorders

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