Sleep deprivation decreases glycogen in the cerebellum  but not in the cortex of young rats

Gip, Phung; Hagiwara, Grace; Ruby, Norman F.; Heller, H. Craig

doi:10.1152/ajpregu.00735.2001

Cited by 50 publications

(61 citation statements)

References 38 publications

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“…The present study and our previous work (15) show that changes in brain glycogen after SD are strongly influenced by age, brain region, and genotype. Most striking was our finding that glycogen increased by 40% in the cortex of B6 mice after SD, while the same treatment had no effect on cortical glycogen in either AK or D2 mice.…”

Section: Discussionsupporting

confidence: 81%

“…Several factors varied among the present study, our previous study (15), and the study of Kong et al (21) that could have contributed to the discrepancies in the Fig. 2.…”

Section: Discussionmentioning

confidence: 50%

“…The methods for the determination of glycogen and glucose have been described in detail elsewhere (15). In all experiments mice were killed by microwave irradiation between 1400 and 1430 using a Gerling-Moore 4101 microwave.…”

Section: Methodsmentioning

confidence: 99%

“…In one study, a decrease in glycogen was observed throughout most of the brain of adult rats sleep deprived for 12 h or longer (21), thus supporting our hypothesis. In a developmental study from our own laboratory, glycogen was found to decrease after sleep deprivation (SD) in the cerebellum but not in the cortex of 24-to 50-day-old rats (15). Moreover, in 59-day-old rats (the oldest age group studied), glycogen increased in the cortex after a 12-h SD and did not change in the cerebellum.…”

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confidence: 92%

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Changes in brain glycogen after sleep deprivation vary with genotype

Franken

Gip

Hagiwara

et al. 2003

American Journal of Physiology-Regulatory, Integrative and Comp

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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 ϳ40% 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.mouse; sleep function and regulation; brain glycogen; glucose; energy homeostasis; food deprivation; halothane anesthesia COMPARED WITH WAKEFULNESS, non-rapid-eye-movement sleep (NREMS) is accompanied by a decrease in brain metabolism (reviewed in Ref. 26). These observations have led to several hypotheses concerning a functional link between sleep and energy homeostasis in the brain. We have advanced a hypothesis integrating both functional and regulatory aspects regarding sleep (3). As to sleep function, we proposed that cerebral glycogen stores, the most important energy store in the brain (19), are progressively depleted during wakefulness and have to be replenished during NREMS. As to sleep regulation, we implicated adenosine as a molecular feedback signal for sleep need (reviewed by Refs. 3,33,35). We proposed that glycogen depletion enhances extracellular adenosine release, thereby promoting sleep onset, sleep continuity, and NREMS delta power [i.e., EEG power in the 1-to 4-Hz range, a marker of NREMS need (5, 6, 12)].A sleep-regulatory role for adenosine has gained considerable support (reviewed by Ref. 33). A functional role for sleep in regulating glycogen content has received less attention. Recently, two studies directly tested this hypothesis by comparing brain glycogen between sleep-deprived and control rats. The results were inconclusive. In one study, a decrease in glycogen was observed throughout most of the brain of adult rats sleep deprived for 12 h or longer (21), thus supporting our hypothesis. In a developmental study from our own laboratory, glycogen was found to decrease after sleep deprivation (SD) in the cerebellum but not in the cortex of 24-to 50-day-old rats (15). Moreover, in 59-day-old rats (the oldest age group studied), glycogen increased i...

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Section: Discussionsupporting

confidence: 81%

“…Several factors varied among the present study, our previous study (15), and the study of Kong et al (21) that could have contributed to the discrepancies in the Fig. 2.…”

Section: Discussionmentioning

confidence: 50%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 92%

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Changes in brain glycogen after sleep deprivation vary with genotype

Franken

Gip

Hagiwara

et al. 2003

American Journal of Physiology-Regulatory, Integrative and Comp

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“…The second aspect of the hypothesis is that sleep, and in particular SWS, might serve to replenish glycogen stores depleted during the waking period. Recent experimental results have failed to verify or falsify this hypothesis, since both (small) decreases and increases in brain glycogen levels have been observed following sleep deprivation (Franken et al, 2003;Gip et al, 2002;Kong et al, 2002).…”

Section: Glycogen Metabolism and Homeostatic Regulation Of Sleepmentioning

confidence: 99%

Neuron–glia metabolic coupling and plasticity

Magistretti

2006

Journal of Experimental Biology

615

399

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Brain energy metabolismBackground The energy requirements of the brain are amazingly high; indeed, while representing only 2% of the body mass, its oxygen and glucose utilization account for approximately 20% of those of the whole organism, almost ten times more than those predicted on a mass basis . A similar mismatch is observed for blood flow destined to the brain, which represents over 10% of cardiac output. In addition to these quantitative aspects, brain metabolism has other distinctive features, in particular its regional variability and the nature of its cellular determinants. At the macroscopic level, one regional variability is manifested by the difference in energy metabolism between grey and white matter (Clarke and Sokoloff, 1994). But a much finer feature of brain metabolism is that its regional variability is strongly determined by the ever-changing spatially and temporally specified levels of synaptic activity. Thus one of the founding principles of brain physiology is that metabolism and flow are tightly coupled with neuronal activity; this fact has been appreciated since the turn of the 19th century when Sherrington proposed that "…the brain possess an intrinsic mechanism by which its vascular supply can be varied locally in correspondence with local variations of functional activity" (Roy and Sherrington, 1890).The pioneering work of Louis Sokoloff and his colleagues in the 1970s and 1980s using the 2-deoxyglucose (2-DG) autoradiographic technique and its in vivo extension to humans with 18-fluoro-DG imaging of glucose utilization by positron emission tomography (PET) (Sokoloff et al., 1977), has clearly demonstrated a similar coupling between neuronal activity and glucose metabolism. Indeed, this tight relationship between neuronal activity with blood flow and metabolism has provided the basis for the functional brain imaging techniques that are now widely in use by cognitive neuroscientists and clinicians (Mazziotta et al., 2000). Thus local changes in glucose utilization, blood flow and oxygen utilization for PET and, mostly, variations in the level of hemoglobin oxygenation for functional magnetic resonance imaging (fMRI) during wellThe coupling between synaptic activity and glucose utilization (neurometabolic coupling) is a central physiological principle of brain function that has provided the basis for 2-deoxyglucose-based functional imaging with positron emission tomography (PET). Astrocytes play a central role in neurometabolic coupling, and the basic mechanism involves glutamate-stimulated aerobic glycolysis; the sodium-coupled reuptake of glutamate by astrocytes and the ensuing activation of the Na-K-ATPase triggers glucose uptake and processing via glycolysis, resulting in the release of lactate from astrocytes. Lactate can then contribute to the activity-dependent fuelling of the neuronal energy demands associated with synaptic transmission. An operational model, the 'astrocyteneuron lactate shuttle', is supported experimentally by a large body of evidence, which provides a molecu...

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Sleep and Waking Across the Life Span

Huber¹,

Tononi

2009

Handbook of Neuroscience for the Behavioral Sciences

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Sleep deprivation decreases glycogen in the cerebellum but not in the cortex of young rats

Cited by 50 publications

References 38 publications

Changes in brain glycogen after sleep deprivation vary with genotype

Changes in brain glycogen after sleep deprivation vary with genotype

Neuron–glia metabolic coupling and plasticity

Sleep and Waking Across the Life Span

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