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Calcineurin is a central regulator of process S and governs sleep homeostasis in locus coeruleus

ABSTRACT: Calcineurin is a central regulator of process S and governs sleep homeostasis in locus coeruleus

PROVIDER: PRJNA1079795 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28074062.fastq.gz	Fastqsanger.gz
	SRR28074063.fastq.gz	Fastqsanger.gz
	SRR28074064.fastq.gz	Fastqsanger.gz
	SRR28074065.fastq.gz	Fastqsanger.gz
	SRR28074066.fastq.gz	Fastqsanger.gz

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Calcineurin is a central regulator of process S and governs sleep homeostasis in locus coeruleus

Project description:Sleep need accumulates during waking and dissipates during sleep to maintain sleep homeostasis (process S). Besides regulation of daily sleep amount, a hallmark of process S is the homeostatic sleep regulation: sleep loss causes increased amount and intensity of subsequent recovery sleep. The central regulators of process S and specific brain regions that govern sleep homeostasis in mammals remain unclear. Here, we report that enhanced calcineurin activity in the mouse brain neurons sharply increases non-rapid eye movement sleep (NREMS) to average ~17-h/day. Knockout of calcineurin in adult mouse brain diminishes baseline NREMS to average ~4-h/day, but also abolishes recovery NREMS owing to inability to accumulate sleep need during wakefulness. Calcineurin promotes baseline NREMS in both excitatory and inhibitory neurons and by antagonizing PKA and activating SIK3 via S551 dephosphorylation. Moreover, calcineurin is specifically required in the locus coeruleus-noradrenergic (LCNA) neurons for the transcriptomic and homeostatic responses to sleep loss. While chemo-/optogenetic activation of LCNA neurons increases the amount and intensity of NREMS, ablation and inhibition of LCNA neurons diminish recovery NREMS following sleep deprivation. These results establish calcineurin as a central regulator of process S and identify LC as a potential sleep need center that governs NREMS homeostasis in mice.

2025-02-28 | GSE256499 | GEO

Discovery of Calcineurin as an Essential Regulator of Sleep

Project description:Research into mechanisms underlying sleep traditionally relies on electrophysiology and genetics. Because sleep can only be measured on whole animals by behavioral observations and physical means, no sleep research was initiated by biochemical and chemical biological approaches. We used phosphorylation sites of kinases important for sleep as targets for biochemical and chemical biological approaches. Sleep was increased in mice carrying a threonine-to-alanine substitution at residue T469 of salt inducible kinase 3 (SIK3). Our biochemical purification and photo-crosslinking revealed calcineurin dephosphorylation, both in vitro and in vivo, of SIK3 at T469 and S551, but not T221. Knocking down calcineurin regulatory subunit reduced daily sleep by more than 5 hours, exceeding all known mouse mutants. Our work uncovered a critical physiological role for calcineurin in sleep and pioneered biochemical purification and chemical biology as effective approaches to study sleep.

2024-12-02 | PXD058505 |

Sleep Deprivation and Recovery Sleep for 7 Regions of Mouse Brain.

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Sleep Deprivation and Recovery Sleep for 7 Regions of Mouse Brain.

Project description:Analysis of the effects of sleep deprivation, recovery sleep, and three time-of-day controls on seven brain regions laser microdissected from mouse brain. The regions include the locus coeruleus, suprachiasmatic nucleus, hypocretin area, tuberomammillary nucleus, orbital cortex, posteromedial cortical amygdala, and entorhinal cortex. In this study, 7 brain regions were collected by laser microdissection from brain tissue of mice from 5 different treatment groups and used for microarray experiments. Four biological replicates were generated for each regionxcondition. Conditions are: SD, sleep deprivation for 6 hours from ZT0 - 6; SDC, time-of-day control for SD at ZT6; RS, recovery sleep for 4 hours following SD; RSC, time-of-day control for RS at ZT10; W, spontaneous waking at ZT18.

2010-08-16 | E-GEOD-23628 | biostudies-arrayexpress

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BDNF-TrkB signaling orchestrates the buildup process for local sleep

Project description:Using pharmacology and optogenetics perturbations, we showed that cortical brain-derived neurotrophic factor (BDNF) regulates the intensity of SWA via the activation of Tyrosine kinase B (TrkB) receptor and cAMP-response element-binding protein (CREB). We identified that the circuitry mediating TrkB-induced sleep SWA involves excitatory pyramidal cells of the cortex's layer 5. We found that increased neuronal firing alone in the somatosensory cortex was not sufficient to increase SWA. Using mathematical modeling of a local network in the brain, we model how BDNF’s effects on synaptic strength can increase SWA in ways not achieved through increased firing alone. Together, our findings implicate BDNF-TrkB-CREB signaling pathway in local SWA control during sleep.

2024-06-22 | PXD045652 | Pride

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