Energy metabolism, ion homeostasis, and cell damage in the brain

1994 ◽  
Vol 22 (4) ◽  
pp. 991-996 ◽  
Author(s):  
Ken-ichiro Katsura ◽  
Tibor Kristián ◽  
Bo K. Siesjö
Keyword(s):  
Energy Metabolism ◽  
Cell Damage ◽  
Ion Homeostasis ◽  
The Brain

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

Improvement of Postischemic Cell Damage and Energy Metabolism in the Rat by Flunarizine and Emopamil

1988 ◽  
pp. 401-402
Author(s):  
D. Sauer ◽  
G. W. Bielenberg ◽  
J. Nuglisch ◽  
T. Beck ◽  
H. D. Mennel ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Cell Damage

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 Myocardial Damage by SARS-CoV-2: Emerging Mechanisms and Therapies

Viruses ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 1880
Author(s):  
Huyen Tran Ho ◽  
Stefan Peischard ◽  
Nathalie Strutz-Seebohm ◽  
Karin Klingel ◽  
Guiscard Seebohm
Keyword(s):  
Immune Response ◽  
Cell Death ◽  
Energy Metabolism ◽  
Programmed Cell Death ◽  
Viral Replication ◽  
Ion Homeostasis ◽  
Membrane Vesicles ◽  
Cardiac Cells ◽  
The Body ◽  
Double Membrane

Evidence is emerging that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can infect various organs of the body, including cardiomyocytes and cardiac endothelial cells in the heart. This review focuses on the effects of SARS-CoV-2 in the heart after direct infection that can lead to myocarditis and an outline of potential treatment options. The main points are: (1) Viral entry: SARS-CoV-2 uses specific receptors and proteases for docking and priming in cardiac cells. Thus, different receptors or protease inhibitors might be effective in SARS-CoV-2-infected cardiac cells. (2) Viral replication: SARS-CoV-2 uses RNA-dependent RNA polymerase for replication. Drugs acting against ssRNA(+) viral replication for cardiac cells can be effective. (3) Autophagy and double-membrane vesicles: SARS-CoV-2 manipulates autophagy to inhibit viral clearance and promote SARS-CoV-2 replication by creating double-membrane vesicles as replication sites. (4) Immune response: Host immune response is manipulated to evade host cell attacks against SARS-CoV-2 and increased inflammation by dysregulating immune cells. Efficiency of immunosuppressive therapy must be elucidated. (5) Programmed cell death: SARS-CoV-2 inhibits programmed cell death in early stages and induces apoptosis, necroptosis, and pyroptosis in later stages. (6) Energy metabolism: SARS-CoV-2 infection leads to disturbed energy metabolism that in turn leads to a decrease in ATP production and ROS production. (7) Viroporins: SARS-CoV-2 creates viroporins that lead to an imbalance of ion homeostasis. This causes apoptosis, altered action potential, and arrhythmia.

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.

Biochemical Effects of Cerebral Ischemia: Relevance To Migraine

Cephalalgia ◽  
1985 ◽  
Vol 5 (2_suppl) ◽  
pp. 35-42 ◽  
Author(s):  
KMA Welch ◽  
JA Helpern ◽  
JR Ewing ◽  
WM Robertson ◽  
G D'Andrea
Keyword(s):  
Energy Metabolism ◽  
Cerebral Ischemia ◽  
Spreading Depression ◽  
Metabolic Depression ◽  
Ischemia And Reperfusion ◽  
Phosphate Metabolism ◽  
Biochemical Effects ◽  
The Brain ◽  
Intracranial Circulation

Although decreased CBF has now been reported during the prodrome of migraine, the cause of the decreased flow is still unknown. It is particularly unclear whether these phenomena are related to vasospasm and “steal” between the extracranial and intracranial circulation or to the spreading depression of Leao and the accompanying metabolic depression. In the present paper, metabolic changes in the brain during ischemia and reperfusion are reviewed and compared with CNS biochemical changes during migraine attack. In addition, the technique of Topical Magnetic Resonance (TMR) as applied to the in vivo study of energy phosphate metabolism in extracranial tissues and brain is described and the potential of this technique to evaluate shifts in energy metabolism and pH in stroke and migraine is discussed.

Slow ATP loss and the defense of ion homeostasis in the anoxic frog brain

2001 ◽  
Vol 204 (20) ◽  
pp. 3547-3551
Author(s):  
Debra L. Knickerbocker ◽  
Peter L. Lutz
Keyword(s):  
Initial Phase ◽  
Ion Homeostasis ◽  
Atp Depletion ◽  
Neuronal Membrane ◽  
Anoxia Tolerance ◽  
Frog Brain ◽  
Atp Levels ◽  
Anoxic Depolarization ◽  
Rate Of Increase ◽  
The Brain

SUMMARY For most vertebrates, cutting off the oxygen supply to the brain results in a rapid (within minutes) loss of ATP, the failure of ATP-dependent ion-transport process, subsequent anoxic depolarization of neuronal membrane potential and consequential neuronal death. The few species that survive brain anoxia for days or months, such as the freshwater turtle Trachemys scripta, avoid anoxic depolarization and maintain brain ATP levels through a coordinated downregulation of brain energy demand processes. The frog Rana pipiens represents an intermediate in anoxia-tolerance, being able to survive brain anoxia for hours. However, the anoxic frog brain does not defend its energy stores. Instead, anoxia-tolerance appears to be related to a retarded rate of ATP depletion. To investigate the relationship between this slow ATP depletion and the loss of ionic homeostasis, cerebral extracellular K+ concentrations were monitored and ATP levels measured during anoxia, during the initial phase of anoxic depolarization and during complete anoxic depolarization. Extracellular K+ levels were maintained at normoxic levels for at least 3 h of anoxia, while ATP content decreased by 35 %. When ATP levels reached 0.33±0.06 mmol l–1 (mean ± s.e.m., N=5), extracellular K+ levels slowly started to increase. This value is thought to represent a critical ATP concentration for the maintenance of ion homeostasis. When extracellular [K+] reached an inflection value of 4.77±0.84 mmol l–1 (mean ± s.e.m., N=5), approximately 1 h later, the brain quickly depolarized. Part of the reduction in ATP demand was attributable to an approximately 50 % decrease in the rate of K+ efflux from the anoxic frog brain, which would also contribute to the retarded rate of increase in extracellular [K+] during the initial phase of anoxic depolarization. However, unlike the anoxia-tolerant turtle brain, adenosine did not appear to be involved in the downregulation of K+ leakage in the frog brain. The increased anoxia-tolerance of the frog brain is thought to be a matter more of slow death than of enhanced protective mechanisms.

Prolonged anoxic survival due to anoxia pre-exposure: brain ATP, lactate, and pyruvate

1964 ◽  
Vol 207 (2) ◽  
pp. 452-456 ◽  
Author(s):  
Nancy Ann Dahl ◽  
William M. Balfour
Keyword(s):  
Energy Metabolism ◽  
Survival Time ◽  
Glucose Concentration ◽  
Prolonged Survival ◽  
Anaerobic Glycolysis ◽  
Cerebral Energy Metabolism ◽  
Atp Concentration ◽  
Lactate And Pyruvate ◽  
The Brain

Rats subjected to a brief anoxia can survive go sec in a second anoxia, compared to a 60-sec survival time of control animals. Slower disappearance of ATP concentration in the brain during the second exposure indicates this longer survival is due to an altered cerebral energy metabolism. Initial cerebral ATP concentration is no higher in pre-exposed animals than in controls. When glycolysis is inhibited by iodoacetate before testing in anoxia, the advantage of pre-exposure disappears, suggesting the longer survival may be due to increased anacrobic glycolysis. Lactate accumulates faster during anoxia in the brains of pre-exposed animals than in controls, suggesting that increased anaerobic glycolysis is the cause of the prolonged survival. This effect is not due to increased cerebral glucose concentration. A possible reason for this increased glycolysis, and thus the prolonged survival, could be an increase of a compound, such as pyruvate, capable of oxidizing NADH. The initial pyruvate is higher in pre-exposed animals than in controls and injection of pyruvate increases the survival time slightly.

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