scholarly journals Adenosine, Energy Metabolism, and Sleep

2003 ◽  
Vol 3 ◽  
pp. 790-798 ◽  
Author(s):  
Tarja Porkka-Heiskanen ◽  
Anna Kalinchuk ◽  
Lauri Alanko ◽  
Anna Urrila ◽  
Dag Stenberg
Keyword(s):  
Energy Metabolism ◽  
Basal Forebrain ◽  
Local Energy ◽  
Energy Depletion ◽  
Exact Function ◽  
Energy Stores ◽  
Function Of Sleep ◽  
The Brain ◽  
Experimentally Induced

While the exact function of sleep remains unknown, it is evident that sleep was developed early in phylogenesis and represents an ancient and vital strategy for survival. Several pieces of evidence suggest that the function of sleep is associated with energy metabolism, saving of energy, and replenishment of energy stores. Prolonged wakefulness induces signs of energy depletion in the brain, while experimentally induced, local energy depletion induces increase in sleep, similarly as would a period of prolonged wakefulness. The key molecule in the induction of sleep appears to be adenosine, which induces sleep locally in the basal forebrain.

The function of sleep

2018 ◽  
Author(s):  
Andrew J. K. Phillips
Keyword(s):  
Immune Function ◽  
Empirical Evidence ◽  
Universal Function ◽  
Metabolic Function ◽  
Sleep Research ◽  
Open Questions ◽  
Energy Stores ◽  
Function Of Sleep ◽  
The Brain

The function of sleep was a longstanding mystery in neuroscience, but there is now compelling empirical evidence for several key functions of sleep. Elucidating these functions and their underlying pathways is a hot area for the field of sleep research today, and many open questions remain. What we have gleaned from recent data is that it is important to view sleep as a synthesis of processes that enable improved functioning during wakefulness. There is no single universal function of sleep, but rather a collection of synergistic functions that are each of varying importance to different species. In humans, sleep plays critical roles in consolidating memories, restoring energy stores in the brain, clearing wastes from the brain, immune function, metabolic function, and overall health.

Local energy depletion in the basal forebrain increases sleep

2003 ◽  
Vol 17 (4) ◽  
pp. 863-869 ◽  
Author(s):  
Anna V. Kalinchuk ◽  
Anna-Sofia Urrila ◽  
Lauri Alanko ◽  
Silja Heiskanen ◽  
Henna-Kaisa Wigren ◽  
...  
Keyword(s):  
Basal Forebrain ◽  
Local Energy ◽  
Energy Depletion

Energy Metabolism and Effects of Energy Depletion or Exposure to Glutamate

1992 ◽  
Vol 70 (S1) ◽  
pp. S107-S112 ◽  
Author(s):  
Louis Sokoloff
Keyword(s):  
Energy Metabolism ◽  
Brain Cells ◽  
Cerebral Hypoxia ◽  
Energy Depletion ◽  
Pathological Conditions ◽  
Oxidative Energy Metabolism ◽  
The Subject ◽  
Tissue Acidosis ◽  
The Brain

The entire program of the first day of the IBRO satellite meeting entitled Ions, Water, and Energy in Brain Cells was devoted to the subject of energy. There were three sessions on the topics of energy metabolism, activation, and development and pathological conditions, followed by a final general discussion on the contents of the day's topics. During this general discussion there were spirited exchanges on the role of glycogen in the energy metabolism of the brain, on the metabolic source of the energy consumed by functional activity, e.g., glycolytic or oxidative energy metabolism, and on the sources of the acid-equivalents that are responsible for the tissue acidosis accompanying cerebral hypoxia. Despite the arguments pro and con presented on all of the issues that were discussed, it is doubtful that a consensus was achieved on most of the issues.Key words: glycogen, glycolysis, oxidative metabolism, acidosis, energy metabolism.

scholarly journals Time to Be SHY? Some Comments on Sleep and Synaptic Homeostasis

2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
Giulio Tononi ◽  
Chiara Cirelli
Keyword(s):  
Synaptic Strength ◽  
Universal Function ◽  
Systematic Bias ◽  
Synaptic Homeostasis ◽  
The Face ◽  
Essential Function ◽  
Function Of Sleep ◽  
The Brain

Sleep must serve an essential, universal function, one that offsets the risk of being disconnected from the environment. The synaptic homeostasis hypothesis (SHY) is an attempt to identify this essential function. Its core claim is that sleep is needed to reestablish synaptic homeostasis, which is challenged by the remarkable plasticity of the brain. In other words, sleep is “the price we pay for plasticity.” In this issue, M. G. Frank reviewed several aspects of the hypothesis and raised several issues. The comments below provide a brief summary of the motivations underlying SHY and clarify that SHY is a hypothesis not about specific mechanisms, but about a universal, essential function of sleep. This function is the preservation of synaptic homeostasis in the face of a systematic bias toward a net increase in synaptic strength—a challenge that is posed by learning during adult wake, and by massive synaptogenesis during development.

Age changes in enzymes of neuronal and microvascular energy metabolism in the brain of spontaneously hypertensive rats

1990 ◽  
Vol 109 (5) ◽  
pp. 682-685
Author(s):  
V. A. Sorokoumov ◽  
Yu. Ya. Kislyakov ◽  
E. L. Pugacheva ◽  
E. R. Barantsevich ◽  
V. A. Grantyn'
Keyword(s):  
Energy Metabolism ◽  
Spontaneously Hypertensive Rats ◽  
Age Changes ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
The Brain

scholarly journals The "selfish brain" hypothesis for metabolic abnormalities in bipolar disorder and schizophrenia

2012 ◽  
Vol 34 (3) ◽  
pp. 121-128 ◽  
Author(s):  
Rodrigo Barbachan Mansur ◽  
Elisa Brietzke
Keyword(s):  
Bipolar Disorder ◽  
Energy Metabolism ◽  
Energy Supply ◽  
Clinical Implications ◽  
Metabolic Abnormalities ◽  
Compensatory Mechanisms ◽  
High Prevalence ◽  
Brain Theory ◽  
The Brain ◽  
Brain Energy

Metabolic abnormalities are frequent in patients with schizophrenia and bipolar disorder (BD), leading to a high prevalence of diabetes and metabolic syndrome in this population. Moreover, mortality rates among patients are higher than in the general population, especially due to cardiovascular diseases. Several neurobiological systems involved in energy metabolism have been shown to be altered in both illnesses; however, the cause of metabolic abnormalities and how they relate to schizophrenia and BD pathophysiology are still largely unknown. The "selfish brain" theory is a recent paradigm postulating that, in order to maintain its own energy supply stable, the brain modulates energy metabolism in the periphery by regulation of both allocation and intake of nutrients. We hypothesize that the metabolic alterations observed in these disorders are a result of an inefficient regulation of the brain energy supply and its compensatory mechanisms. The selfish brain theory can also expand our understanding of stress adaptation and neuroprogression in schizophrenia and BD, and, overall, can have important clinical implications for both illnesses.

scholarly journals Glycolytically impaired glial cells fuel neural metabolism via β-oxidation

2021 ◽  
Author(s):  
Stefanie Schirmeier ◽  
Helen Hertenstein ◽  
Ellen McMullen ◽  
Leon Deharde ◽  
Marko Brankatschk
Keyword(s):  
Glial Cells ◽  
Brain Function ◽  
Ketone Bodies ◽  
Carbohydrate Restriction ◽  
Neuronal Function ◽  
Adverse Conditions ◽  
Energy Stores ◽  
Metabolic Sensor ◽  
The Brain ◽  
Starvation Conditions

Abstract Neuronal function is highly energy demanding and thus requires efficient and constant metabolite delivery. Like their mammalian counterparts Drosophila glia are highly glycolytic and provide lactate to fuel neuronal metabolism. However, flies are able to survive for several weeks in the absence of glial glycolysis1. Here, we study how glial cells maintain sufficient nutrient supply to neurons under conditions of carbohydrate restriction. We show that glycolytically impaired glia switch to fatty acid breakdown via β-oxidation and provide ketone bodies as an alternate neuronal fuel. Moreover, flies also rely on glial β-oxidation under starvation conditions with glial loss of β-oxidation increasing susceptibility to starvation. Further, we show that glial cells act as a metabolic sensor in the brain and can induce mobilization of peripheral energy stores to ensure brain metabolic homeostasis. In summary, our study gives pioneering evidence on the importance of glial β-oxidation and ketogenesis for brain function, and survival, under adverse conditions, like malnutrition. The glial capacity to utilize lipids as an energy source seems to be conserved from flies to humans.

scholarly journals Sleeping While Awake: The Intrusion of Neural Activity Associated with Sleep Onset in the Awake Human Brain

2020 ◽  
Author(s):  
Stephanie Hawes ◽  
Carrie R. H. Innes ◽  
Nicholas Parsons ◽  
Sean P.A. Drummond ◽  
Karen Caeyensberghs ◽  
...  
Keyword(s):  
Human Brain ◽  
Basal Forebrain ◽  
Brain Activity ◽  
Cognitive Task ◽  
Sleep Onset ◽  
Theoretical Modelling ◽  
Related Activity ◽  
Independent Dataset ◽  
Time Graph ◽  
The Brain

AbstractSleep can intrude into the awake human brain when sleep deprived or fatigued, even while performing cognitive tasks. However, how the brain activity associated with sleep onset can co-exist with the activity associated with cognition in the awake humans remains unexplored. Here, we used simultaneous fMRI and EEG to generate fMRI activity maps associated with EEG theta (4-7 Hz) activity associated with sleep onset. We implemented a method to track these fMRI activity maps in individuals performing a cognitive task after well-rested and sleep-deprived nights. We found frequent intrusions of the fMRI maps associated with sleep-onset in the task-related fMRI data. These sleep events elicited a pattern of transient fMRI activity, which was spatially distinct from the task-related activity in the frontal and parietal areas of the brain. They were concomitant with reduced arousal as indicated by decreased pupil size and increased response time. Graph theoretical modelling showed that the activity associated with sleep onset emerges from the basal forebrain and spreads anterior-posteriorly via the brain’s structural connectome. We replicated the key findings in an independent dataset, which suggests that the approach can be reliably used in understanding the neuro-behavioural consequences of sleep and circadian disturbances in humans.

scholarly journals Aspartoacylase Supports Oxidative Energy Metabolism during Myelination

2012 ◽  
Vol 32 (9) ◽  
pp. 1725-1736 ◽  
Author(s):  
Jeremy S Francis ◽  
Louise Strande ◽  
Vladamir Markov ◽  
Paola Leone
Keyword(s):  
Energy Metabolism ◽  
Postnatal Development ◽  
Strong Association ◽  
Canavan Disease ◽  
Lipid Synthesis ◽  
Systematic Analysis ◽  
Early Postnatal Development ◽  
Neuronal Viability ◽  
Oxidative Energy Metabolism ◽  
The Brain

The inherited leukodystrophy Canavan disease arises due to a loss of the ability to catabolize N-acetylaspartic acid (NAA) in the brain and constitutes a major point of focus for efforts to define NAA function. Accumulation of noncatabolized NAA is diagnostic for Canavan disease, but contrasts with the abnormally low NAA associated with compromised neuronal integrity in a broad spectrum of other clinical conditions. Experimental evidence for NAA function supports a role in white matter lipid synthesis, but does not explain how both elevated and lowered NAA can be associated with pathology in the brain. We have undertaken a systematic analysis of postnatal development in a mouse model of Canavan disease that delineates development and pathology by identifying markers of oxidative stress preceding oligodendrocyte loss and dysmyelination. These data suggest a role for NAA in the maintenance of metabolic integrity in oligodendrocytes that may be of relevance to the strong association between NAA and neuronal viability. N-acetylaspartic acid is proposed here to support lipid synthesis and energy metabolism via the provision of substrate for both cellular processes during early postnatal development.

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