Calcium Oscillation Frequency-Sensitive Gene Regulation and Homeostatic Compensation in Pancreatic $$\upbeta $$-Cells

Yildirim, Vehpi; Bertram, Richard

doi:10.1007/s11538-017-0286-1

Cited by 8 publications

(7 citation statements)

References 79 publications

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“…Lightman and colleagues (Spiga et al., ) have developed mathematical models to explore the interaction between the circadian clock and this ultradian endocrine rhythm. Furthermore, a mathematical modelling study of pancreatic islet β‐cells has shown that calcium‐dependent transcription can adjust potassium channel activity to rescue electrical bursting and insulin oscillations (Yildirim & Bertram, ). Circadian rhythms also modulate cortical excitability and EEG synchrony (Ly et al., ).…”

Section: Modelling Section 4: Future Directions For Mathematical Modementioning

confidence: 99%

Neuronal oscillations on an ultra‐slow timescale: daily rhythms in electrical activity and gene expression in the mammalian master circadian clockwork

Belle

Diekman

2018

Eur J of Neuroscience

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Neuronal oscillations of the brain, such as those observed in the cortices and hippocampi of behaving animals and humans, span across wide frequency bands, from slow delta waves (0.1 Hz) to ultra-fast ripples (600 Hz). Here, we focus on ultra-slow neuronal oscillators in the hypothalamic suprachiasmatic nuclei (SCN), the master daily clock that operates on interlocking transcription-translation feedback loops to produce circadian rhythms in clock gene expression with a period of near 24 h (< 0.001 Hz). This intracellular molecular clock interacts with the cell's membrane through poorly understood mechanisms to drive the daily pattern in the electrical excitability of SCN neurons, exhibiting an up-state during the day and a down-state at night. In turn, the membrane activity feeds back to regulate the oscillatory activity of clock gene programs. In this review, we emphasise the circadian processes that drive daily electrical oscillations in SCN neurons, and highlight how mathematical modelling contributes to our increasing understanding of circadian rhythm generation, synchronisation and communication within this hypothalamic region and across other brain circuits.

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Section: Modelling Section 4: Future Directions For Mathematical Modementioning

confidence: 99%

Neuronal oscillations on an ultra‐slow timescale: daily rhythms in electrical activity and gene expression in the mammalian master circadian clockwork

Belle

Diekman

2018

Eur J of Neuroscience

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“…These features include spike frequency during the burst, dynamics during the silent phase (oscillatory or not), shape of the burst (on a plateau compared to the silent phase or, on the contrary, with undershoots). These 3 features led Rinzel to name 3 classes: square-wave bursting , observed in a number of recordings and models of pancreatic beta-cells [ 47 ] among other [ 48 ]; elliptic bursting , observed in various neural recordings and models of sensory neurons [ 15 , 49 ]; and parabolic bursting , initially observed in the Aplysia R15 neuron [ 42 ] and ever since in various neural models [ 50 ]. We show an example of each class in Fig 4 .…”

Section: Introductionmentioning

confidence: 99%

Classification of bursting patterns: A tale of two ducks

2022

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Bursting is one of the fundamental rhythms that excitable cells can generate either in response to incoming stimuli or intrinsically. It has been a topic of intense research in computational biology for several decades. The classification of bursting oscillations in excitable systems has been the subject of active research since the early 1980s and is still ongoing. As a by-product, it establishes analytical and numerical foundations for studying complex temporal behaviors in multiple timescale models of cellular activity. In this review, we first present the seminal works of Rinzel and Izhikevich in classifying bursting patterns of excitable systems. We recall a complementary mathematical classification approach by Bertram and colleagues, and then by Golubitsky and colleagues, which, together with the Rinzel-Izhikevich proposals, provide the state-of-the-art foundations to these classifications. Beyond classical approaches, we review a recent bursting example that falls outside the previous classification systems. Generalizing this example leads us to propose an extended classification, which requires the analysis of both fast and slow subsystems of an underlying slow-fast model and allows the dissection of a larger class of bursters. Namely, we provide a general framework for bursting systems with both subthreshold and superthreshold oscillations. A new class of bursters with at least 2 slow variables is then added, which we denote folded-node bursters, to convey the idea that the bursts are initiated or annihilated via a folded-node singularity. Key to this mechanism are so-called canard or duck orbits, organizing the underpinning excitability structure. We describe the 2 main families of folded-node bursters, depending upon the phase (active/spiking or silent/nonspiking) of the bursting cycle during which folded-node dynamics occurs. We classify both families and give examples of minimal systems displaying these novel bursting patterns. Finally, we provide a biophysical example by reinterpreting a generic conductance-based episodic burster as a folded-node burster, showing that the associated framework can explain its subthreshold oscillations over a larger parameter region than the fast subsystem approach.

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“…Bursting oscillations play an integral role in insulin secretion by pancreatic -cells 84 , and these cells can compensate for genetic deletions of a critical channel K(ATP) channel population by over-expressing other potassium channels 86 in the mouse, but not in humans. Recent work suggests that these cells can use intracellular calcium as a sensor of voltage dynamics in a negative feedback loop to regulate activity 87 . Thus, many other cell types may share common features of homeostatic regulation with neurons such as robustness to size changes and sensitivity to some perturbations 88 .…”

Section: Discussionmentioning

confidence: 99%

Activity-dependent compensation of cell size is vulnerable to targeted deletion of ion channels

Gorur-Shandilya

Marder

O’Leary

2020

Sci Rep

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In many species, excitable cells preserve their physiological properties despite significant variation in physical size across time and in a population. For example, neurons in crustacean central pattern generators generate similar firing patterns despite several-fold increases in size between juveniles and adults. This presents a biophysical problem because the electrical properties of cells are highly sensitive to membrane area and channel density. It is not known whether specific mechanisms exist to sense membrane area and adjust channel expression to keep a consistent channel density, or whether regulation mechanisms that sense activity alone are capable of compensating cell size. We show that destabilising effects of growth can be specifically compensated by feedback mechanism that senses average calcium influx and jointly regulate multiple conductances. However, we further show that this class of growth-compensating regulation schemes is necessarily sensitive to perturbations that alter the expression of subsets of ion channel types. Targeted perturbations of specific ion channels can trigger a pathological response of the regulation mechanism and a failure of homeostasis. Our findings suggest that physiological regulation mechanisms that confer robustness to growth may be specifically vulnerable to deletions or mutations that affect subsets of ion channels.

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Calcium Oscillation Frequency-Sensitive Gene Regulation and Homeostatic Compensation in Pancreatic $$\upbeta $$-Cells

Cited by 8 publications

References 79 publications

Neuronal oscillations on an ultra‐slow timescale: daily rhythms in electrical activity and gene expression in the mammalian master circadian clockwork

Neuronal oscillations on an ultra‐slow timescale: daily rhythms in electrical activity and gene expression in the mammalian master circadian clockwork

Classification of bursting patterns: A tale of two ducks

Activity-dependent compensation of cell size is vulnerable to targeted deletion of ion channels

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