scholarly journals A role for astroglial calcium in mammalian sleep

2019 ◽  
Author(s):  
Ashley M. Ingiosi ◽  
Christopher R. Hayworth ◽  
Daniel O. Harvey ◽  
Kristan G. Singletary ◽  
Michael J. Rempe ◽  
...  
Keyword(s):  
Sleep Deprivation ◽  
Intracellular Calcium ◽  
Neuronal Activity ◽  
Brain Cells ◽  
Sleep Regulation ◽  
Natural Sleep ◽  
Sleep Homeostat ◽  
Homeostatic Response

AbstractMammalian sleep is characterized by dramatic changes in neuronal activity, and waking neuronal activity is thought to increase sleep need. Changes in other brain cells (glia) across the natural sleep-wake cycle and their role in sleep regulation are comparatively unexplored. We show that sleep is also accompanied by large changes in astroglial activity as measured by intracellular calcium concentrations in unanesthetized mice. These changes in calcium vary across different vigilance states and are most pronounced in distal astroglial processes. We find that reducing intracellular calcium in astrocytes impaired the homeostatic response to sleep deprivation. Thus, astroglial calcium changes dynamically across vigilance states and is a component of the sleep homeostat.One Sentence SummaryAstroglial calcium concentrations vary with sleep and wake, change after sleep deprivation, and mediate sleep need.

Homeostatic Response to Sleep Restriction in Adolescents

SLEEP ◽  
2021 ◽  
Author(s):  
Jelena Skorucak ◽  
Nathan Weber ◽  
Mary A Carskadon ◽  
Chelsea Reynolds ◽  
Scott Coussens ◽  
...  
Keyword(s):  
Slow Wave ◽  
Process Model ◽  
Animal Studies ◽  
Sleep Restriction ◽  
Sleep Regulation ◽  
Homeostatic Process ◽  
Sleep Homeostasis ◽  
High Prevalence ◽  
Homeostatic Response ◽  
Chronic Sleep

Abstract The high prevalence of chronic sleep restriction in adolescents underscores the importance of understanding how adolescent sleep is regulated under such conditions. One component of sleep regulation is a homeostatic process: if sleep is restricted, then sleep intensity increases. Our knowledge of this process is primarily informed by total sleep deprivation studies and has been incorporated in mathematical models of human sleep regulation. Several animal studies, however, suggest that adaptation occurs in chronic sleep restriction conditions, showing an attenuated or even decreased homeostatic response. We investigated the homeostatic response of adolescents to different sleep opportunities. Thirty-four participants were allocated to one of three groups with 5, 7.5 or 10 h of sleep opportunity per night for 5 nights. Each group underwent a protocol of 9 nights designed to mimic a school week between 2 weekends: 2 baseline nights (10 h sleep opportunity), 5 condition nights (5, 7.5 or 10 h), and two recovery nights (10 h). Measures of sleep homeostasis (slow-wave activity and slow-wave energy) were calculated from frontal and central EEG derivations and compared to predictions derived from simulations of the homeostatic process of the two-process model of sleep regulation. Only minor differences were found between empirical data and model predictions, indicating that sleep homeostasis is preserved under chronic sleep restriction in adolescents. These findings improve our understanding of effects of repetitive short sleep in adolescents.

Sleep after arousal from hibernation is not homeostatically regulated

1999 ◽  
Vol 276 (2) ◽  
pp. R522-R529 ◽  
Author(s):  
Jennie E. Larkin ◽  
H. Craig Heller
Keyword(s):  
Sleep Deprivation ◽  
Brain Function ◽  
Extended Period ◽  
Nrem Sleep ◽  
Wave Activity ◽  
Ground Squirrels ◽  
Recovery Sleep ◽  
Sleep Homeostasis ◽  
Homeostatic Response ◽  
Periodic Arousals

Electroencephalographic slow-wave activity (SWA) in non-rapid eye movement (NREM) sleep is directly related to prior sleep/wake history, with high levels of SWA following extended periods of wake. Therefore, SWA has been thought to reflect the level of accumulated sleep need. The discovery that euthermic intervals between hibernation bouts are spent primarily in sleep and that this sleep is characterized by high and monotonically declining SWA has led to speculation that sleep homeostasis may play a fundamental role in the regulation of the timing of bouts of hibernation and periodic arousals to euthermia. It was proposed that because the SWA profile seen after arousal from hibernation is strikingly similar to what is seen in nonhibernating mammals after extended periods of wakefulness, that hibernating mammals may arouse from hibernation with significant accumulated sleep need. This sleep need may accumulate during hibernation because the low brain temperatures during hibernation may not be compatible with sleep restorative processes. In the present study, golden-mantled ground squirrels were sleep deprived during the first 4 h of interbout euthermia by injection of caffeine (20 mg/kg ip). We predicted that if the SWA peaks after bouts of hibernation reflected a homeostatic response to an accumulated sleep need, sleep deprivation should simply have displaced and possibly augmented the SWA to subsequent recovery sleep. Instead we found that after caffeine-induced sleep deprivation of animals just aroused from hibernation, the anticipated high SWA typical of recovery sleep did not occur. Similar results were found in a study that induced sleep deprivation by gentle handling (19). These findings indicate that the SWA peak immediately after hibernation does not represent homeostatic regulation of NREM sleep, as it normally does after prolonged wakefulness during euthermia, but instead may reflect some other neurological process in the recovery of brain function from an extended period at low temperature.

Down-regulation of free intracellular calcium in dissociated brain cells of aged mice and rats

Life Sciences ◽  
1996 ◽  
Vol 59 (5-6) ◽  
pp. 435-449 ◽  
Author(s):  
Henrike Hartmann ◽  
Anne Eckert ◽  
Karsten Velbinger ◽  
Michael Rewsin ◽  
Walter E. Müller
Keyword(s):  
Intracellular Calcium ◽  
Brain Cells ◽  
Down Regulation ◽  
Aged Mice ◽  
Free Intracellular Calcium ◽  
Dissociated Brain Cells

Changes in brain glycogen after sleep deprivation vary with genotype

2003 ◽  
Vol 285 (2) ◽  
pp. R413-R419 ◽  
Author(s):  
Paul Franken ◽  
Phung Gip ◽  
Grace Hagiwara ◽  
Norman F. Ruby ◽  
H. Craig Heller
Keyword(s):  
Sleep Deprivation ◽  
Brain Stem ◽  
Energy Homeostasis ◽  
Glycogen Content ◽  
Inbred Strains ◽  
Sleep Regulation ◽  
Compensatory Response ◽  
Glucose Content ◽  
Brain Glycogen ◽  
Brain Energy

Sleep has been functionally implicated in brain energy homeostasis in that it could serve to replenish brain energy stores that become depleted while awake. Sleep deprivation (SD) should therefore lower brain glycogen content. We tested this hypothesis by sleep depriving mice of three inbred strains, i.e., AKR/J (AK), DBA/2J (D2), and C57BL/6J (B6), that differ greatly in their sleep regulation. After a 6-h SD, these mice and their controls were killed by microwave irradiation, and glycogen and glucose were quantified in the cerebral cortex, brain stem, and cerebellum. After SD, both measures significantly increased by ∼40% in the cortex of B6 mice, while glycogen significantly decreased by 20–38% in brain stem and cerebellum of AK and D2 mice. In contrast, after SD, glucose content increased in all three structures in AK mice and did not change in D2 mice. The increase in glycogen after SD in B6 mice persisted under conditions of food deprivation that, by itself, lowered cortical glycogen. Furthermore, the strains that differ most in their compensatory response to sleep loss, i.e., AK and D2, did not differ in their glycogen response. Thus glycogen content per se is an unlikely end point of sleep's functional role in brain energy homeostasis.

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.

Intracellular calcium recordings from isolated cells of the mammalian central nervous system

1987 ◽  
Vol 65 (5) ◽  
pp. 926-933 ◽  
Author(s):  
M. E. Morris ◽  
J. F. MacDonald ◽  
J. J. Friedlich ◽  
I. Szekelyhidi
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Intracellular Calcium ◽  
Mouse Embryo ◽  
Dorsal Root Ganglion Neurons ◽  
Brain Cells ◽  
Isolated Cells ◽  
Mammalian Central Nervous System ◽  
Intracellular Ca ◽  
Ganglion Neurons

Measurements made with two different techniques of intracellular calcium levels from small isolated cells of the mammalian central nervous system are described and compared. Recordings in cultured mouse embryo spinal cord and dorsal root ganglion neurons, made with double-barrelled borosilicate Ca2+-selective microelectrodes yielded a mean Ca2+ level of 2.3 (SE ± 0.54) μM for the lowest values recorded in 24 out of 46 cells. Intracellular Ca2+ dependence on membrane potential was apparent with levels of calcium ≥4 μM (r = 0.371, n = 29). Both cyclic fluctuations induced by tetraethylammonium and an apparent increase in Ca2+ evoked by the depolarizing excitatory amino acid, L-aspartate, were observed. In contrast, estimates of intracellular Ca2+ obtained by spectrofluorimetry of suspensions of mouse embryo brain cells, loaded with the intracellular Ca-binding fluorescent probe, quin2 provided a [Formula: see text]-fold lower value, 152 (SE ± 7) nM. This more closely resembles levels reported for large neurons where large-tip microelectrodes with greater sensitivity were used, and in spite of the heterogeneity of the cells this value is presumed to be a more accurate estimate of intraneuronal Ca2+ concentration. In these fluorescence studies KCl readily evoked increases in intracellular Ca2+ which could be blocked by verapamil and Cd2+ and were not induced in the absence of Ca2+. Increases were also produced by N-methyl-D-aspartate, but not by the kainate-like Lathyrus neurotoxin, L-3-oxalylamino-2-aminopropionic acid. These results provide preliminary evidence for both voltage-sensitive and receptor-activated Ca channels in embryonic brain cells. Although the recording of intraneuronal Ca2+ with conventional ion-selective microelectrodes in small cells has problems with respect to accuracy, stability, and time constant, recent advances in the design of Ca2+ sensors and electrodes are promising. These, as well as developments in techniques of single cell fluorescence analysis, now offer methods with improved and powerful capacity for accurate and simultaneous measurements of intracellular Ca2+ and membrane electrophysiological parameters.

Sleep regulation in rats: effects of sleep deprivation, light, and circadian phase

1986 ◽  
Vol 251 (6) ◽  
pp. R1037-R1044 ◽  
Author(s):  
L. Trachsel ◽  
I. Tobler ◽  
A. A. Borbely
Keyword(s):  
Sleep Deprivation ◽  
Slow Wave Sleep ◽  
Rest Period ◽  
Activity Period ◽  
Base Line ◽  
Sleep Regulation ◽  
Continuous Darkness ◽  
Circadian Phase ◽  
Sleep Homeostasis ◽  
Pentobarbital Sodium Anesthesia

Sleep states and electroencephalographic (EEG) parameters were determined in unrestrained rats that had been implanted with electrodes under deep pentobarbital sodium anesthesia. Two base-line days with a light-dark cycle (LD) and 2 days under continuous darkness (DD) were followed by 24 h of sleep deprivation (SD) ending in the middle of the circadian activity period and by 2 recovery days in DD. In the base-line LD rest period, the amount of rapid-eye-movement sleep (REMS) and the EEG amplitude of non-REMS (NREMS) were lower than in the corresponding DD period. SD caused an immediate enhancement of REMS, NREMS, the slow-wave sleep (SWS) fraction of NREMS, and NREMS EEG amplitude. Although REMS, NREMS, and SWS showed a second peak at habitual light onset, they did not exceed base line. Subsequently, all parameters exhibited a marked negative rebound. We conclude that REMS and the EEG amplitude of NREMS are suppressed by light, amplitude and frequency parameters of NREMS are differently affected by light as well as by SD, and the short duration of the SD-induced increase of SWS may reflect a circadian influence on sleep homeostasis.

scholarly journals EphA4 is Involved in Sleep Regulation but Not in the Electrophysiological Response to Sleep Deprivation

SLEEP ◽  
2016 ◽  
Vol 39 (3) ◽  
pp. 613-624 ◽  
Author(s):  
Marlène Freyburger ◽  
Audrey Pierre ◽  
Gabrielle Paquette ◽  
Erika Bélanger-Nelson ◽  
Joseph Bedont ◽  
...  
Keyword(s):  
Sleep Deprivation ◽  
Sleep Regulation ◽  
Electrophysiological Response

The cycad neurotoxic amino acid, ß-N-methylamino-l-alanine (BMAA), elevates intracellular calcium levels in dissociated rat brain cells

2002 ◽  
Vol 82 (2-3) ◽  
pp. 159-167 ◽  
Author(s):  
Delia M Brownson ◽  
Tom J Mabry ◽  
Steven W Leslie
Keyword(s):  
Amino Acid ◽  
Intracellular Calcium ◽  
Rat Brain ◽  
Brain Cells

scholarly journals Protein lactylation induced by neural excitation

2021 ◽  
Author(s):  
Hideo Hagihara ◽  
Hirotaka Shoji ◽  
Hikari Otabi ◽  
Atsushi Toyoda ◽  
Kaoru Katoh ◽  
...  
Keyword(s):  
Neuronal Activity ◽  
Monocarboxylate Transporter ◽  
Brain Cells ◽  
Post Translational Modification ◽  
High Potassium ◽  
Neural Excitation ◽  
Lactate Levels ◽  
The Brain ◽  
Prefrontal Cortices

AbstractLactate is known to have diverse roles in the brain at the molecular and behavioral levels under both physiological and pathophysiological conditions, such as learning and memory and regulation of mood. Recently, a novel post-translational modification called lysine lactylation has been found in histone H3 of mouse macrophages, and the lactylation levels paralleled the intracellular lactate levels1. However, it is unknown whether lysine lactylation occurs in brain cells, and if it does, whether lactylation is induced by the stimuli that accompany changes in lactate levels. Herein, we reveal that lysine lactylation in brain cells is regulated by systemic changes in lactate levels, neural excitation, and behaviorally relevant stimuli. Lysine lactylation levels were increased by lactate treatment and by high-potassium-induced depolarization in cultured primary neurons; these increases were attenuated by pharmacological inhibition of monocarboxylate transporter 2 and lactate dehydrogenase, respectively, suggesting that both cell-autonomous and non-cell-autonomous neuronal mechanisms are involved in overall lysine lactylation. In vivo, electroconvulsive stimulation increased lysine lactylation levels in the prefrontal cortices of mice, and its levels were positively correlated with the expression levels of the neuronal activity marker c-Fos on an individual cell basis. In the social defeat stress model of depression in which brain lactate levels increase, lactylation levels were increased in the prefrontal cortices of the defeated mice, which was accompanied by increased c-Fos expression, decreased social behaviors, and increased anxiety-like behaviors, suggesting that stress-induced neuronal excitation may induce lysine lactylation, thereby affecting mood-related behaviors. Further, we identified 63 candidate lysine-lactylated proteins in the mouse cortex and found that lactylation levels in histone H1 increased in response to defeat stress. This study may open up an avenue for exploration of a novel role of neuronal activity-induced lactate mediated by protein lactylation in the brain.

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