The Experts below are selected from a list of 294 Experts worldwide ranked by ideXlab platform

Menno P Gerkema - One of the best experts on this subject based on the ideXlab platform.

  • unmasking Ultradian rhythms in gene expression
    The FASEB Journal, 2017
    Co-Authors: Daan R Van Der Veen, Menno P Gerkema
    Abstract:

    Biological oscillations with an Ultradian time scale of 1 to several hours include cycles in behavioral arousal, episodic glucocorticoid release, and gene expression. Ultradian rhythms are thought to have an extrinsic origin because of a perceived absence of Ultradian rhythmicity in vitro and a lack of known molecular Ultradian oscillators. We designed a novel, non-spectral-analysis method of separating Ultradian from circadian components and applied it to a published gene expression dataset with an Ultradian sampling resolution. Ultradian rhythms in mouse hepatocytes in vivo have been published, and we validated our approach using this control by confirming 175 of 323 Ultradian genes identified in a prior study and found 862 additional Ultradian genes. For the first time, we now report Ultradian expression of >900 genes in vitro Sixty genes exhibited Ultradian transcriptional rhythmicity, both in vivo and in vitro, including 5 genes involved in the cell cycle. Within these 60 genes, we identified significant enrichment of specific DNA motifs in the 1000 bp proximal promotor, some of which associate with known transcriptional factors. These findings are in strong support of instrinsically driven Ultradian rhythms and expose potential molecular mechanisms and functions underlying Ultradian rhythms that remain unknown.-Van der Veen, D. R., Gerkema, M. P. Unmasking Ultradian rhythms in gene expression.

  • impact of behavior on central and peripheral circadian clocks in the common vole microtus arvalis a mammal with Ultradian rhythms
    Proceedings of the National Academy of Sciences of the United States of America, 2006
    Co-Authors: Daan R Van Der Veen, Menno P Gerkema, Nguyet Le Minh, Milica Arneric, Ulrich Schibler
    Abstract:

    In most mammals, daily rhythms in physiology are driven by a circadian timing system composed of a master pacemaker in the suprachiasmatic nucleus (SCN) and peripheral oscillators in most body cells. The SCN clock, which is phase-entrained by light–dark cycles, is thought to synchronize subsidiary oscillators in peripheral tissues, mainly by driving cyclic feeding behavior. Here, we examined the expression of circadian clock genes in the SCN and the liver of the common vole Microtus arvalis, a rodent with Ultradian activity and feeding rhythms. In these animals, clock-gene mRNAs accumulate with high circadian amplitudes in the SCN but are present at nearly constant levels in the liver. Interestingly, high-amplitude circadian liver gene expression can be elicited by subjecting voles to a circadian feeding regimen. Moreover, voles with access to a running wheel display a composite pattern of circadian and Ultradian behavior, which correlates with low-amplitude circadian gene expression in the liver. Our data indicate that, in M. arvalis, the amplitude of circadian liver gene expression depends on the contribution of circadian and Ultradian components in activity and feeding rhythms.

  • phase control of Ultradian feeding rhythms in the common vole microtus arvalis the roles of light and the circadian system
    Journal of Biological Rhythms, 1993
    Co-Authors: Menno P Gerkema, Serge Daan, Marieke Wilbrink, Floris Van Der Leest
    Abstract:

    In their Ultradian (2- to 3-hr) feeding rhythm, common voles show intraindividual synchrony from day to day, as well as interindividual synchrony between members of the population, even at remote distances. This study addresses the question of how resetting of the Ultradian rhythm, a prerequisite for such synchronization, is achieved. Common voles were subjected to short light-dark cycles (1 hr darkness with light varying between 0.7 and 2.5 hr); to T cycles (long light-dark cycles in the circadian range—16 hr darkness and 3-13 hr light); to light pulses (15 min) during different circadian and Ultradian phases; and to addition of D2O to the drinking water (25%). Short light-dark cycles and D2O were also applied to voles without circadian rhythmicity, after lesions of the suprachiasmatic nuclei. In these experiments, four hypotheses on synchronization of Ultradian rhythmicity were tested: (I) synchronization by a direct response to light; (II) synchronization via the circadian system with multiple triggers, here called "cogs," each controlling a single Ultradian feeding bout; and (III and IV) synchronization via the circadian system with a single "cog," which resets an Ultradian oscillator and either (III) originates directly from the circadian pacemaker, or (IV) is mediated via the overt circadian activity rhythm. Short light-dark cycles failed to entrain Ultradian rhythms, either in circadian-rhythmic or in non-circadian-rhythmic voles; light pulses did not cause phase shifts; and in extreme T cycles no stable phase relationship with light could be demonstrated. Thus, Hypothesis I was rejected. Changes in the circadian period (τ) were generated as aftereffects of light pulses, by entrainment in various T cycles, and by the addition of D2O to the drinking water. These changes in τ did not lead to parallel, let alone proportional, changes in the Ultradian period. This excluded Hypothesis II. Both in T-cycle experiments and in the D2O experiments with circadian-rhythmic voles, the phase of Ultradian feeding bouts was locked to the end of circadian activity rather than to the most prominent marker of the pacemaker, the onset of circadian activity. This was not expected under Hypothesis III, but was consistent with entrainment via activity (Hypothesis IV). On the basis of these experiments, we conclude that the most likely mechanism of Ultradian entrainment is that of a light-insensitive Ultradian oscillator, reset every dawn by the termination of the activity phase controlled by the circadian pacemaker, which is itself entrained by the light-dark cycle. Neither in circadian-rhythmic nor in non-circadian-rhythmic voles was the period of the feeding rhythm lengthened by administration of D2O. This insensitivity to deuterium is exceptional among biological rhythms.

Stafford L Lightman - One of the best experts on this subject based on the ideXlab platform.

  • Chapter 43 – Ultradian Rhythms
    Stress: Neuroendocrinology and Neurobiology, 2020
    Co-Authors: Francesca Spiga, J. Pooley, Georgina M Russell, Stafford L Lightman
    Abstract:

    The hypothalamic-pituitary-adrenal (HPA) axis regulates circulating levels of glucocorticoid hormones to provide a rapid response and defense against stress. Under basal (i.e., unstressed) conditions, glucocorticoids are released with an Ultradian pattern that results in rapid Ultradian oscillations of hormone levels both in the blood and within target tissues, including the brain. In this review we discuss the origin and regulation of Ultradian HPA rhythm, both at system levels and at the level of the adrenal cortex, how it affects the physiology of the organism, both at transcriptional and behavioral levels, and what its clinical relevance is.

  • circadian and Ultradian glucocorticoid rhythmicity implications for the effects of glucocorticoids on neural stem cells and adult hippocampal neurogenesis
    Frontiers in Neuroendocrinology, 2016
    Co-Authors: Carlos P Fitzsimons, J Herbert, M Schouten, Onno C Meijer, Paul J Lucassen, Stafford L Lightman
    Abstract:

    Total glucocorticoid hormone levels in plasma of various species, including humans, follow a circadian rhythm that is made up from an underlying series of hormone pulses. In blood most of the glucocorticoid is bound to corticosteroid-binding globulin and albumin, resulting in low levels of free hormone. Although only the free fraction is biologically active, surprisingly little is known about the rhythms of free glucocorticoid hormones. We used single-probe microdialysis to measure directly the free corticosterone levels in the blood of freely behaving rats. Free corticosterone in the blood shows a distinct circadian and Ultradian rhythm with a pulse frequency of approximately one pulse per hour together with an increase in hormone levels and pulse height toward the active phase of the light/dark cycle. Similar rhythms were also evident in the subcutaneous tissue, demonstrating that free corticosterone rhythms are transferred from the blood into peripheral target tissues. Furthermore, in a dual-probe microdialysis study, we demonstrated that the circadian and Ultradian rhythms of free corticosterone in the blood and the subcutaneous tissue were highly synchronized. Moreover, free corticosterone rhythms were also synchronous between the blood and the hippocampus. These data demonstrate for the first time an Ultradian rhythm of free corticosterone in the blood that translates into synchronized rhythms of free glucocorticoid hormone in peripheral and central tissues. The maintenance of Ultradian rhythms across tissue barriers in both the periphery and the brain has important implications for research into aberrant biological rhythms in disease and for the development of improved protocols for glucocorticoid therapy.

  • Ultradian corticosterone secretion is maintained in the absence of circadian cues
    European Journal of Neuroscience, 2012
    Co-Authors: Eleanor Waite, M A Mckenna, Y M Kershaw, Jamie J Walker, Hugh D Piggins, Stafford L Lightman
    Abstract:

    : Plasma levels of corticosterone exhibit both circadian and Ultradian rhythms. The circadian component of these rhythms is regulated by the suprachiasmatic nucleus (SCN). Our studies investigate the importance of the SCN in regulating Ultradian rhythmicity. Two approaches were used to dissociate the hypothalamic-pituitary-adrenal (HPA) axis from normal circadian input in rats: (i) exposure to a constant light (LL) environment and (ii) electrolytic lesioning of the SCN. Blood was sampled using an automated sampling system. As expected, both treatments resulted in a loss of the circadian pattern of corticosterone secretion. Ultradian pulsatile secretion of corticosterone however, was maintained across the 24 h in all animals. Furthermore, the loss of SCN input revealed an underlying relationship between locomotor and HPA activity. In control (LD) rats there was no clear correlation between Ultradian locomotor activity and hormone secretion, whereas, in LL rats, episodes of Ultradian activity were consistently followed by periods of increased pulsatile hormone secretion. These data clearly demonstrate that the Ultradian rhythm of corticosterone secretion is generated through a mechanism independent of the SCN input, supporting recent evidence for a sub-hypothalamic pulse generator.

  • the hsp90 molecular chaperone cycle regulates cyclical transcriptional dynamics of the glucocorticoid receptor and its coregulatory molecules cbp p300 during Ultradian ligand treatment
    Molecular Endocrinology, 2011
    Co-Authors: Becky L Conwaycampbell, John R Pooley, Gordon L Hager, Charlotte L George, David M Knight, Michael Norman, Stafford L Lightman
    Abstract:

    HSP90 regulates cyclical glucocorticoid receptor activity, cofactor recruitment, histone acetylation and transcriptional pulsing at the Period 1 promoter in response to Ultradian glucocorticoid exposure.

  • recovery from disrupted Ultradian glucocorticoid rhythmicity reveals a dissociation between hormonal and behavioural stress responsiveness
    Journal of Neuroendocrinology, 2010
    Co-Authors: R A Sarabdjitsingh, Y M Kershaw, Stafford L Lightman, Francesca Spiga, Onno C Meijer, Melly S Oitzl, E R De Kloet
    Abstract:

    Ultradian release of glucocorticoids is thought to be essential for homeostasis and health. Furthermore, deviation from this pulsatile release pattern is considered to compromise resilience to stress-related disease, even after hormone levels have normalised. In the present study, we investigate how constant exposure to different concentrations of corticosterone affects diurnal and Ultradian pulsatility. The rate of recovery in pulsatile hypothalamic-pituitary-adrenal (HPA) activity after withdrawal of exogenous corticosterone is also examined. Finally, the behavioural and neuroendocrine responsiveness to an audiogenic stressor is studied. Adrenally intact male rats were subcutaneously implanted with vehicle, 40% or 100% corticosterone pellets for 7 days. The continuous release of corticosterone from these implants abolished diurnal and Ultradian corticosterone variation, as measured with high-frequency automated blood sampling. Pellet removal on post-surgery day 8 allowed rapid recovery of endogenous rhythms in animals previously exposed to daily average concentrations (40%) but not after exposure to high concentrations (100%) of corticosterone. Behavioural and neuroendocrine responsiveness to stress was distinctly different between the treatment groups. Audiogenic stimulation 1 day after pellet removal resulted in a similar corticosterone response in animals previously exposed to 40% corticosterone or vehicle. The 40% pellet group, however, showed less and shorter behavioural activity (i.e. locomotion, risk assessment) to noise stress compared to 100% corticosterone and vehicle-treated animals. In conclusion, unlike the animals impanted with 100% corticosterone, we find that basal HPA axis activity in the 40% group, which had mean daily levels of circulating corticosterone in the physiological range, rapidly reverts to the characteristic pulsatile pattern of corticosterone secretion. Upon reinstatement of the Ultradian rhythm, and despite the fact that these animals did not differ from controls in their response to noise stress, they did show substantial changes in their behavioural response to stress.

Akifumi Kishi - One of the best experts on this subject based on the ideXlab platform.

  • markov modeling of sleep stage transitions and Ultradian rem sleep rhythm
    Physiological Measurement, 2018
    Co-Authors: Akifumi Kishi, Ikuhiro Yamaguchi, Fumiharu Togo, Yoshiharu Yamamoto
    Abstract:

    Objective: One of the highly characteristic features of sleep is the cyclic occurrence of non-rapid eye movement (NREM) and REM sleep, which is referred to as the Ultradian rhythm of sleep. Even though REM sleep was discovered over half a century ago, surprisingly, the mechanism of the Ultradian REM sleep rhythm has not yet been fully elucidated. In the present study, we aim to provide a mechanistic insight into the generation of the Ultradian REM sleep rhythm. Approach and Main results: By simulating hypnograms with the dynamic features of sleep stage transitions, i.e. stage transition probabilities and stage-specific survival time functions, we show that the second-order Markov transition probabilities and the stage-specific survival time functions can reproduce the central position (~90 min) of the REM-onset intervals (ROIs), but with a larger variance in distribution. In addition, we demonstrate the direct effect of the increased probability of the transitions from light to deep sleep within NREM sleep on the prolongation of the ROIs in a dose-response manner. Significance: These results suggest that dynamic sleep stage transitions constitute the basis of the formation of the Ultradian rhythm of sleep; however, further elaboration of the model would be required to reduce the variability in rhythmicity.

  • nrem sleep stage transitions control Ultradian rem sleep rhythm
    Sleep, 2011
    Co-Authors: Akifumi Kishi, Hideaki Yasuda, Takahisa Matsumoto, Yasushi Inami, Jun Horiguchi, Masako Tamaki, Zbigniew R Struzik, Yoshiharu Yamamoto
    Abstract:

    Study Objectives: The cyclic sequence of NReM and ReM sleep, the so-called Ultradian rhythm, is a highly characteristic feature of sleep. However, the mechanisms responsible for the Ultradian ReM sleep rhythm, particularly in humans, have not to date been fully elucidated. We hypothesize that a stage transition mechanism is involved in the determination of the Ultradian ReM sleep rhythm. Participants: Ten healthy young male volunteers (age: 22 ± 4 years, range 19-31 years) spent 3 nights in a sleep laboratory. The first was the adaptation night, and the second was the baseline night. on the third night, the subjects received risperidone (1 mg tablet), a central serotonergic and dopaminergic antagonist, 30 min before the polysomnography recording. Measurements and Results: We measured and investigated transition probabilities between waking, ReM, and NReM sleep stages (N1, N2, and N3) within the ReM-onset intervals, defined as the intervals between the onset of one ReM period and the beginning of the next, altered by risperidone. We also calculated the transition intensity (i.e., instantaneous transition rate) and examined the temporal pattern of transitions within the altered ReM-onset intervals. We found that when the ReM-onset interval was prolonged by risperidone, the probability of transitions from N2 to N3 was significantly increased within the same prolonged interval, with a significant delay and/or recurrences of the peak intensity of transitions from N2 to N3. Conclusions: These results suggest that the mechanism governing NReM sleep stage transitions (from light to deep sleep) plays an important role in determining Ultradian ReM sleep rhythms.

Daan R Van Der Veen - One of the best experts on this subject based on the ideXlab platform.

  • unmasking Ultradian rhythms in gene expression
    The FASEB Journal, 2017
    Co-Authors: Daan R Van Der Veen, Menno P Gerkema
    Abstract:

    Biological oscillations with an Ultradian time scale of 1 to several hours include cycles in behavioral arousal, episodic glucocorticoid release, and gene expression. Ultradian rhythms are thought to have an extrinsic origin because of a perceived absence of Ultradian rhythmicity in vitro and a lack of known molecular Ultradian oscillators. We designed a novel, non-spectral-analysis method of separating Ultradian from circadian components and applied it to a published gene expression dataset with an Ultradian sampling resolution. Ultradian rhythms in mouse hepatocytes in vivo have been published, and we validated our approach using this control by confirming 175 of 323 Ultradian genes identified in a prior study and found 862 additional Ultradian genes. For the first time, we now report Ultradian expression of >900 genes in vitro Sixty genes exhibited Ultradian transcriptional rhythmicity, both in vivo and in vitro, including 5 genes involved in the cell cycle. Within these 60 genes, we identified significant enrichment of specific DNA motifs in the 1000 bp proximal promotor, some of which associate with known transcriptional factors. These findings are in strong support of instrinsically driven Ultradian rhythms and expose potential molecular mechanisms and functions underlying Ultradian rhythms that remain unknown.-Van der Veen, D. R., Gerkema, M. P. Unmasking Ultradian rhythms in gene expression.

  • impact of behavior on central and peripheral circadian clocks in the common vole microtus arvalis a mammal with Ultradian rhythms
    Proceedings of the National Academy of Sciences of the United States of America, 2006
    Co-Authors: Daan R Van Der Veen, Menno P Gerkema, Nguyet Le Minh, Milica Arneric, Ulrich Schibler
    Abstract:

    In most mammals, daily rhythms in physiology are driven by a circadian timing system composed of a master pacemaker in the suprachiasmatic nucleus (SCN) and peripheral oscillators in most body cells. The SCN clock, which is phase-entrained by light–dark cycles, is thought to synchronize subsidiary oscillators in peripheral tissues, mainly by driving cyclic feeding behavior. Here, we examined the expression of circadian clock genes in the SCN and the liver of the common vole Microtus arvalis, a rodent with Ultradian activity and feeding rhythms. In these animals, clock-gene mRNAs accumulate with high circadian amplitudes in the SCN but are present at nearly constant levels in the liver. Interestingly, high-amplitude circadian liver gene expression can be elicited by subjecting voles to a circadian feeding regimen. Moreover, voles with access to a running wheel display a composite pattern of circadian and Ultradian behavior, which correlates with low-amplitude circadian gene expression in the liver. Our data indicate that, in M. arvalis, the amplitude of circadian liver gene expression depends on the contribution of circadian and Ultradian components in activity and feeding rhythms.

Yoshiharu Yamamoto - One of the best experts on this subject based on the ideXlab platform.

  • markov modeling of sleep stage transitions and Ultradian rem sleep rhythm
    Physiological Measurement, 2018
    Co-Authors: Akifumi Kishi, Ikuhiro Yamaguchi, Fumiharu Togo, Yoshiharu Yamamoto
    Abstract:

    Objective: One of the highly characteristic features of sleep is the cyclic occurrence of non-rapid eye movement (NREM) and REM sleep, which is referred to as the Ultradian rhythm of sleep. Even though REM sleep was discovered over half a century ago, surprisingly, the mechanism of the Ultradian REM sleep rhythm has not yet been fully elucidated. In the present study, we aim to provide a mechanistic insight into the generation of the Ultradian REM sleep rhythm. Approach and Main results: By simulating hypnograms with the dynamic features of sleep stage transitions, i.e. stage transition probabilities and stage-specific survival time functions, we show that the second-order Markov transition probabilities and the stage-specific survival time functions can reproduce the central position (~90 min) of the REM-onset intervals (ROIs), but with a larger variance in distribution. In addition, we demonstrate the direct effect of the increased probability of the transitions from light to deep sleep within NREM sleep on the prolongation of the ROIs in a dose-response manner. Significance: These results suggest that dynamic sleep stage transitions constitute the basis of the formation of the Ultradian rhythm of sleep; however, further elaboration of the model would be required to reduce the variability in rhythmicity.

  • nrem sleep stage transitions control Ultradian rem sleep rhythm
    Sleep, 2011
    Co-Authors: Akifumi Kishi, Hideaki Yasuda, Takahisa Matsumoto, Yasushi Inami, Jun Horiguchi, Masako Tamaki, Zbigniew R Struzik, Yoshiharu Yamamoto
    Abstract:

    Study Objectives: The cyclic sequence of NReM and ReM sleep, the so-called Ultradian rhythm, is a highly characteristic feature of sleep. However, the mechanisms responsible for the Ultradian ReM sleep rhythm, particularly in humans, have not to date been fully elucidated. We hypothesize that a stage transition mechanism is involved in the determination of the Ultradian ReM sleep rhythm. Participants: Ten healthy young male volunteers (age: 22 ± 4 years, range 19-31 years) spent 3 nights in a sleep laboratory. The first was the adaptation night, and the second was the baseline night. on the third night, the subjects received risperidone (1 mg tablet), a central serotonergic and dopaminergic antagonist, 30 min before the polysomnography recording. Measurements and Results: We measured and investigated transition probabilities between waking, ReM, and NReM sleep stages (N1, N2, and N3) within the ReM-onset intervals, defined as the intervals between the onset of one ReM period and the beginning of the next, altered by risperidone. We also calculated the transition intensity (i.e., instantaneous transition rate) and examined the temporal pattern of transitions within the altered ReM-onset intervals. We found that when the ReM-onset interval was prolonged by risperidone, the probability of transitions from N2 to N3 was significantly increased within the same prolonged interval, with a significant delay and/or recurrences of the peak intensity of transitions from N2 to N3. Conclusions: These results suggest that the mechanism governing NReM sleep stage transitions (from light to deep sleep) plays an important role in determining Ultradian ReM sleep rhythms.