scholarly journals Author response: Global sleep homeostasis reflects temporally and spatially integrated local cortical neuronal activity

2020 ◽  
Author(s):  
Christopher W Thomas ◽  
Mathilde CC Guillaumin ◽  
Laura E McKillop ◽  
Peter Achermann ◽  
Vladyslav V Vyazovskiy
Keyword(s):  
Neuronal Activity ◽  
Author Response ◽  
Sleep Homeostasis

scholarly journals Global sleep homeostasis reflects temporally and spatially integrated local cortical neuronal activity

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Christopher W Thomas ◽  
Mathilde CC Guillaumin ◽  
Laura E McKillop ◽  
Peter Achermann ◽  
Vladyslav V Vyazovskiy
Keyword(s):  
Neuronal Activity ◽  
Wave Activity ◽  
Neuronal Firing ◽  
Daily Amount ◽  
Local Process ◽  
Sleep Homeostasis ◽  
Freely Behaving ◽  
Electroencephalogram Eeg ◽  
Activity Dependent ◽  
Wake State

Sleep homeostasis manifests as a relative constancy of its daily amount and intensity. Theoretical descriptions define ‘Process S’, a variable with dynamics dependent on global sleep-wake history, and reflected in electroencephalogram (EEG) slow wave activity (SWA, 0.5–4 Hz) during sleep. The notion of sleep as a local, activity-dependent process suggests that activity history must be integrated to determine the dynamics of global Process S. Here, we developed novel mathematical models of Process S based on cortical activity recorded in freely behaving mice, describing local Process S as a function of the deviation of neuronal firing rates from a locally defined set-point, independent of global sleep-wake state. Averaging locally derived Processes S and their rate parameters yielded values resembling those obtained from EEG SWA and global vigilance states. We conclude that local Process S dynamics reflects neuronal activity integrated over time, and global Process S reflects local processes integrated over space.

scholarly journals Sleep homeostasis reflects temporally integrated local cortical neuronal activity

2019 ◽  
Author(s):  
Christopher W. Thomas ◽  
Mathilde C. C. Guillaumin ◽  
Laura E. McKillop ◽  
Peter Achermann ◽  
Vladyslav V. Vyazovskiy
Keyword(s):  
Neuronal Activity ◽  
Explicit Knowledge ◽  
Neuronal Firing ◽  
Activity Levels ◽  
Homeostatic Regulation ◽  
Sleep Homeostasis ◽  
Species Specific ◽  
Electroencephalogram Eeg ◽  
Wake State ◽  
Relevant Quantity

AbstractThe homeostatic regulation of sleep manifests as a relative constancy of its daily amount and intensity. Theoretical descriptions of this phenomenon define “Process S”, a variable with dynamics dependent only on sleep-wake history, whose levels are reflected in electroencephalogram (EEG) slow wave activity (0.5 – 4 Hz) during sleep. Here we developed novel mathematical models of Process S in mice, assuming that its dynamics are a function of the deviation of cortical neuronal firing rates from a locally defined set-point, crucially without explicit knowledge of sleep-wake state. Our results suggest that Process S tracks global sleep-wake history through an integration of local cortical neuronal activity levels over time. We posit that, instead of reflecting sleep-wake-dependent changes in specific variables and serving their homeostatic regulation, Process S may be a time-keeping mechanism which enables individuals to obtain a species-specific and ecologically-relevant quantity of sleep, even in the absence of external temporal information.

scholarly journals Author response: Regulation of sleep homeostasis by sexual arousal

2017 ◽  
Author(s):  
Esteban J Beckwith ◽  
Quentin Geissmann ◽  
Alice S French ◽  
Giorgio F Gilestro
Keyword(s):  
Sexual Arousal ◽  
Author Response ◽  
Sleep Homeostasis

scholarly journals Cortical neuronal activity does not regulate sleep homeostasis

Neuroscience ◽  
2015 ◽  
Vol 297 ◽  
pp. 211-218 ◽  
Author(s):  
M.-H. Qiu ◽  
M.C. Chen ◽  
J. Lu
Keyword(s):  
Neuronal Activity ◽  
Sleep Homeostasis

scholarly journals Author response: Transitioning between preparatory and precisely sequenced neuronal activity in production of a skilled behavior

2019 ◽  
Author(s):  
Vamsi K Daliparthi ◽  
Ryosuke O Tachibana ◽  
Brenton G Cooper ◽  
Richard HR Hahnloser ◽  
Satoshi Kojima ◽  
...  
Keyword(s):  
Neuronal Activity ◽  
Author Response

scholarly journals Author response: AANAT1 functions in astrocytes to regulate sleep homeostasis

2020 ◽  
Author(s):  
Sejal Davla ◽  
Gregory Artiushin ◽  
Yongjun Li ◽  
Daryan Chitsaz ◽  
Sally Li ◽  
...  
Keyword(s):  
Author Response ◽  
Sleep Homeostasis

scholarly journals The neuropeptide Galanin is required for homeostatic rebound sleep following increased neuronal activity

2018 ◽  
Author(s):  
Sabine Reichert ◽  
Oriol Pavón Arocas ◽  
Jason Rihel
Keyword(s):  
Neuronal Activity ◽  
Sleep Time ◽  
Drug Induced ◽  
Extracellular Signal Regulated Kinase ◽  
Larval Zebrafish ◽  
Sleep Homeostasis ◽  
Extracellular Signal ◽  
Sleep Homeostat ◽  
Activity Marker ◽  
Molecular Signals

AbstractSleep pressure homeostatically increases during wake and dissipates during sleep, but the molecular signals and neuronal substrates that measure homeostatic sleep pressure remain poorly understood. We present a pharmacological assay in larval zebrafish that generates acute, short-term increases in wakefulness followed by sustained rebound sleep after washout. The intensity of global neuronal activity during drug-induced wakefulness predicted the amount of subsequent rebound sleep. Whole brain mapping with the neuronal activity marker phosphorylated extracellular signal–regulated kinase (pERK) identified preoptic Galanin-expressing neurons as selectively active during rebound sleep, and the relative induction of galanin transcripts was predictive of total rebound sleep time. Galanin is required for sleep homeostasis, as galanin mutants almost completely lacked rebound sleep following both pharmacologically induced neuronal activity and physical sleep deprivation. These results suggest that Galanin plays a key role in responding to sleep pressure signals derived from neuronal activity and functions as an output arm of the vertebrate sleep homeostat. (word count: 158).

scholarly journals Paternally expressed imprinted Snord116 and Peg3 regulate hypothalamic orexin neurons

2019 ◽  
Author(s):  
Pace Marta ◽  
Falappa Matteo ◽  
Freschi Andrea ◽  
Balzani Edoardo ◽  
Berteotti Chiara ◽  
...  
Keyword(s):  
Neuronal Activity ◽  
Lateral Hypothalamus ◽  
Rem Sleep ◽  
Neurodevelopmental Disorder ◽  
Imprinted Genes ◽  
List Type ◽  
State Dependent ◽  
Sleep Homeostasis ◽  
Melanin Concentrating Hormone

AbstractImprinted genes are highly expressed in the hypothalamus; however, whether specific imprinted genes affect hypothalamic neuromodulators and their functions is unknown. It has been suggested that Prader-Willi syndrome (PWS), a neurodevelopmental disorder caused by lack of paternal expression at chromosome 15q11-q13, is characterised by hypothalamic insufficiency. Here, we investigate the role of the paternally expressed Snord116 gene within the context of sleep and metabolic abnormalities of PWS, and we report a novel role of this imprinted gene in the function and organisation of the two main neuromodulatory systems of the lateral hypothalamus (LH), namely, the orexin (OX) and melanin concentrating hormone (MCH) systems. We observe that the dynamics between neuronal discharge in the LH and the sleep-wake states of mice with paternal deletion of Snord116 (PWScrm+/p−) are compromised. This abnormal state-dependent neuronal activity is paralleled by a significant reduction in OX neurons in the LH of mutants. Therefore, we propose that an imbalance between OX- and MCH-expressing neurons in the LH of mutants reflects a series of deficits manifested in the PWS, such as dysregulation of rapid eye movement (REM) sleep, food intake and temperature control.HighlightsSnord116 regulates neuronal activity in the lateral hypothalamus (LH), which is time-locked with cortical states of sleep.Loss of Snord116 reduces orexin neurons in the LH and affects sleep homeostasis and thermoregulation in mice.Snord116 and Peg3 independently control orexin expression in the LH.Paternally expressed alleles maximize the patrilineal effects in the control of REM sleep by the LH in mammals.

Sign in / Sign up

Export Citation Format

Share Document