Daily Electrical Silencing in the Mammalian Circadian Clock

Belle, Mino D. C.; Diekman, Casey O.; Forger, Daniel B.; Piggins, Hugh D.

doi:10.1126/science.1169657

Cited by 159 publications

(266 citation statements)

References 25 publications

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“…This trend is consistent with findings of Nygård et al (2005). Depolarized membrane states have been shown recently to silence SCN neurons in the middle of the day in per1-expressing cells (Belle et al, 2009), but, in our data, the mean V m of the silent cells did not differ from mean V m of active cells in any of the groups. Cell capacitance of SCN neurons was significantly reduced in old compared with young animals (Fig.…”

Section: Patch-clamp Recordings Membrane Properties and Excitabilitysupporting

confidence: 82%

Evidence for Neuronal Desynchrony in the Aged Suprachiasmatic Nucleus Clock

Farajnia¹,

Michel²,

Deboer³

et al. 2012

J. Neurosci.

198

212

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Aging is associated with a deterioration of daily (circadian) rhythms in physiology and behavior. Deficits in the function of the central circadian pacemaker in the suprachiasmatic nucleus (SCN) have been implicated, but the responsible mechanisms have not been clearly delineated. In this report, we characterize the progression of rhythm deterioration in mice to 900 d of age. Longitudinal behavioral and sleep-wake recordings in up to 30-month-old mice showed strong fragmentation of rhythms, starting at the age of 700 d. Patch-clamp recordings in this age group revealed deficits in membrane properties and GABAergic postsynaptic current amplitude. A selective loss of circadian modulation of fast delayed-rectifier and A-type K ϩ currents was observed. At the tissue level, phase synchrony of SCN neurons was grossly disturbed, with some subpopulations peaking in anti-phase and a reduction in amplitude of the overall multiunit activity rhythm. We propose that aberrant SCN rhythmicity in old animals-with electrophysiological arrhythmia at the single-cell level and phase desynchronization at the network level-can account for defective circadian function with aging.

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Section: Patch-clamp Recordings Membrane Properties and Excitabilitysupporting

confidence: 82%

Evidence for Neuronal Desynchrony in the Aged Suprachiasmatic Nucleus Clock

Farajnia¹,

Michel²,

Deboer³

et al. 2012

J. Neurosci.

198

212

View full text Add to dashboard Cite

show abstract

“…One possibility is that, unlike cortical networks, continuous presence of action potentials is not essential for intercellular communication. This is demonstrated by the electrical self-silencing of Per1 SCN neurons, which occurs at the supposed peak of their electrical firing (Belle et al, 2009). This could explain why the oscillator cluster structure is sustained even under action potential silencing, as it does not deviate severely from natural conditions.…”

Section: Discussionmentioning

confidence: 99%

Period Coding of Bmal1 Oscillators in the Suprachiasmatic Nucleus

Myung¹,

Hong

Hatanaka

et al. 2012

Journal of Neuroscience

121

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Together with computer simulations, we show that either the intercellular coupling does not strongly influence the Bmal1 oscillation or the nature of the coupling is more complex than previously assumed. Furthermore, we have found that the region-specific periods are modulated by the light conditions that an animal is exposed to. Based on these, we suggest that the period forms the basis of seasonal coding in the SCN.

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“…3). The firing pattern of the SCN neuron was reported to differ between the cells which expressed Per1-GFP and those which did not 27 . These findings suggest that the cell networks of the SCN differ for the cell populations expressing Per1-luc and PER2::LUC.…”

Section: Discussionmentioning

confidence: 99%

Cryptochromes are critical for the development of coherent circadian rhythms in the mouse suprachiasmatic nucleus

2013

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Cryptochrome (Cry) 1 and Cry2 are regarded as critical components for circadian rhythm generation in mammals. Nevertheless, cultured suprachiasmatic nucleus (SCN) of neonatal Cry double deficient (Cry1 À / À /Cry2 À / À ) mice exhibit circadian rhythms that damp out in several cycles. Here, by combining bioluminescence imaging of Per1-luc and PER2::LUC with multielectrode recording, we show developmental changes in SCN circadian rhythms in Cry1 À / À /Cry2 À / À mice. At the tissue level, circadian rhythms are found in neonatal but not in adult SCN, whereas at the cellular level, rhythms are detected in both SCN. Cellular circadian rhythms are synchronized in neonates, but not in adults, indicating a loss of rhythm synchrony in the course of development. Synchronized circadian rhythms in adult Cry1 À / À / Cry2 À / À SCN are restored by coculture of neonatal, but not of juvenile, SCN. These findings indicate that CRY1 and CRY2 are necessary for the development of intercellular networks that subserve coherent rhythm expression in adult SCN.

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Daily Electrical Silencing in the Mammalian Circadian Clock

Cited by 159 publications

References 25 publications

Evidence for Neuronal Desynchrony in the Aged Suprachiasmatic Nucleus Clock

Evidence for Neuronal Desynchrony in the Aged Suprachiasmatic Nucleus Clock

Period Coding of Bmal1 Oscillators in the Suprachiasmatic Nucleus

Cryptochromes are critical for the development of coherent circadian rhythms in the mouse suprachiasmatic nucleus

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