scholarly journals Sleep homeostasis and the circadian clock: Do the circadian pacemaker and the sleep homeostat influence each other’s functioning?

2018 ◽  
Vol 5 ◽  
pp. 68-77 ◽  
Author(s):  
Tom Deboer
Keyword(s):  
Circadian Clock ◽  
Circadian Pacemaker ◽  
Sleep Homeostasis ◽  
Sleep Homeostat

scholarly journals Differential regulation of the Drosophila sleep homeostat by circadian and arousal inputs

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Jinfei D Ni ◽  
Adishthi S Gurav ◽  
Weiwei Liu ◽  
Tyler H Ogunmowo ◽  
Hannah Hackbart ◽  
...  
Keyword(s):  
Circadian Clock ◽  
Differential Regulation ◽  
Central Complex ◽  
Synaptic Connections ◽  
Circadian Pacemaker ◽  
Pacemaker Neurons ◽  
Synaptic Inputs ◽  
Shaped Body ◽  
Sleep Homeostat ◽  
The Brain

One output arm of the sleep homeostat in Drosophila appears to be a group of neurons with projections to the dorsal fan-shaped body (dFB neurons) of the central complex in the brain. However, neurons that regulate the sleep homeostat remain poorly understood. Using neurogenetic approaches combined with Ca2+ imaging, we characterized synaptic connections between dFB neurons and distinct sets of upstream sleep-regulatory neurons. One group of the sleep-promoting upstream neurons is a set of circadian pacemaker neurons that activates dFB neurons via direct glutaminergic excitatory synaptic connections. Opposing this population, a group of arousal-promoting neurons downregulates dFB axonal output with dopamine. Co-activating these two inputs leads to frequent shifts between sleep and wake states. We also show that dFB neurons release the neurotransmitter GABA and inhibit octopaminergic arousal neurons. We propose that dFB neurons integrate synaptic inputs from distinct sets of upstream sleep-promoting circadian clock neurons, and arousal neurons.

Hugin+ neurons provide a link between sleep homeostat and circadian clock neurons

2021 ◽  
Vol 118 (47) ◽  
pp. e2111183118
Author(s):  
Jessica E. Schwarz ◽  
Anna N. King ◽  
Cynthia T. Hsu ◽  
Annika F. Barber ◽  
Amita Sehgal
Keyword(s):  
Locomotor Activity ◽  
Sleep Deprivation ◽  
Circadian Clock ◽  
Sleep Loss ◽  
Daily Cycle ◽  
Shaped Body ◽  
Recovery Sleep ◽  
Sleep Homeostat ◽  
Central Clock ◽  
Homeostatic Mechanisms

Sleep is controlled by homeostatic mechanisms, which drive sleep after wakefulness, and a circadian clock, which confers the 24-h rhythm of sleep. These processes interact with each other to control the timing of sleep in a daily cycle as well as following sleep deprivation. However, the mechanisms by which they interact are poorly understood. We show here that hugin+ neurons, previously identified as neurons that function downstream of the clock to regulate rhythms of locomotor activity, are also targets of the sleep homeostat. Sleep deprivation decreases activity of hugin+ neurons, likely to suppress circadian-driven activity during recovery sleep, and ablation of hugin+ neurons promotes sleep increases generated by activation of the homeostatic sleep locus, the dorsal fan-shaped body (dFB). Also, mutations in peptides produced by the hugin+ locus increase recovery sleep following deprivation. Transsynaptic mapping reveals that hugin+ neurons feed back onto central clock neurons, which also show decreased activity upon sleep loss, in a Hugin peptide–dependent fashion. We propose that hugin+ neurons integrate circadian and sleep signals to modulate circadian circuitry and regulate the timing of sleep.

Mammalian Circadian Clock and Its Resetting

Physiology ◽  
1991 ◽  
Vol 6 (3) ◽  
pp. 129-134
Author(s):  
H Illnerova
Keyword(s):  
Circadian Rhythm ◽  
Circadian Clock ◽  
Complex Structure ◽  
Day Length ◽  
Circadian Pacemaker ◽  
Melatonin Production

Data on resetting circadian rhythm in melatonin production suggest a complex structure of the underlying pacemaker and explain why the circadian pacemaker functions also as a calendar measuring day length. The pacemaker is entrainable not only by light but by various drugs as well.

Gap Junctions Between Accessory Medulla Neurons Appear to Synchronize Circadian Clock Cells of the Cockroach Leucophaea maderae

2006 ◽  
Vol 95 (3) ◽  
pp. 1996-2002 ◽  
Author(s):  
Nils-Lasse Schneider ◽  
Monika Stengl
Keyword(s):  
Gap Junctions ◽  
Circadian Clock ◽  
Phase Difference ◽  
Temporal Organization ◽  
Stable Phase ◽  
Circadian Pacemaker ◽  
Potential Oscillations ◽  
Synaptic Release ◽  
Accessory Medulla ◽  
Leucophaea Maderae

The temporal organization of physiological and behavioral states is controlled by circadian clocks in apparently all eukaryotic organisms. In the cockroach Leucophaea maderae lesion and transplantation studies located the circadian pacemaker in the accessory medulla (AMe). The AMe is densely innervated by γ-aminobutyric acid (GABA)–immunoreactive and peptidergic neurons, among them the pigment-dispersing factor immunoreactive circadian pacemaker candidates. The large majority of cells of the cockroach AMe spike regularly and synchronously in the gamma frequency range of 25–70 Hz as a result of synaptic and nonsynaptic coupling. Although GABAergic coupling forms assemblies of phase-locked cells, in the absence of synaptic release the cells remain synchronized but fire now at a stable phase difference. To determine whether these coupling mechanisms of AMe neurons, which are independent of synaptic release, are based on electrical synapses between the circadian pacemaker cells the gap-junction blockers halothane, octanol, and carbenoxolone were used in the presence and absence of synaptic transmission. Here, we show that different populations of AMe neurons appear to be coupled by gap junctions to maintain synchrony at a stable phase difference. This synchronization by gap junctions is a prerequisite to phase-locked assembly formation by synaptic interactions and to synchronous gamma-type action potential oscillations within the circadian clock.

scholarly journals Bright morning light advances the human circadian system without affecting NREM sleep homeostasis

1989 ◽  
Vol 256 (1) ◽  
pp. R106-R111 ◽  
Author(s):  
D. J. Dijk ◽  
D. G. Beersma ◽  
S. Daan ◽  
A. J. Lewy
Keyword(s):  
Rem Sleep ◽  
Process Model ◽  
Sleep Onset ◽  
Light Condition ◽  
Bright Light ◽  
Circadian Pacemaker ◽  
Sleep Regulation ◽  
Plasma Melatonin ◽  
Sleep Homeostasis ◽  
Dim Light

Eight male subjects were exposed to either bright light or dim light between 0600 and 0900 h for 3 consecutive days each. Relative to the dim light condition, the bright light treatment advanced the evening rise in plasma melatonin and the time of sleep termination (sleep onset was held constant) for an average approximately 1 h. The magnitude of the advance of the plasma melatonin rise was dependent on its phase in dim light. The reduction in sleep duration was at the expense of rapid-eye-movement (REM) sleep. Spectral analysis of the sleep electroencephalogram (EEG) revealed that the advance of the circadian pacemaker did not affect EEG power densities between 0.25 and 15.0 Hz during either non-REM or REM sleep. The data show that shifting the human circadian pacemaker by 1 h does not affect non-REM sleep homeostasis. These findings are in accordance with the predictions of the two-process model of sleep regulation.

scholarly journals Genesis of the Master Circadian Pacemaker in Mice

2021 ◽  
Vol 15 ◽  
Author(s):  
Arthur H. Cheng ◽  
Hai-Ying Mary Cheng
Keyword(s):  
Locomotor Activity ◽  
Body Temperature ◽  
Circadian Clock ◽  
Suprachiasmatic Nucleus ◽  
Temporal Information ◽  
Circadian Pacemaker ◽  
Extrinsic Factors ◽  
Peripheral Oscillators ◽  
Endocrine Signaling ◽  
Intrinsic And Extrinsic Factors

The suprachiasmatic nucleus (SCN) of the hypothalamus is the central circadian clock of mammals. It is responsible for communicating temporal information to peripheral oscillators via humoral and endocrine signaling, ultimately controlling overt rhythms such as sleep-wake cycles, body temperature, and locomotor activity. Given the heterogeneity and complexity of the SCN, its genesis is tightly regulated by countless intrinsic and extrinsic factors. Here, we provide a brief overview of the development of the SCN, with special emphasis on the murine system.

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).

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