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 Glutamate dehydrogenase is essential to sustain neuronal oxidative energy metabolism during stimulation

2017 ◽  
Vol 38 (10) ◽  
pp. 1754-1768 ◽  
Author(s):  
Michaela C Hohnholt ◽  
Vibe H Andersen ◽  
Jens V Andersen ◽  
Sofie K Christensen ◽  
Melis Karaca ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Glutamate Dehydrogenase ◽  
Energy Demand ◽  
Glucose Deprivation ◽  
Brain Mitochondria ◽  
Glutamine Metabolism ◽  
Oxidative Deamination ◽  
Oxidative Energy Metabolism ◽  
The Brain

The enzyme glutamate dehydrogenase (GDH; Glud1) catalyzes the (reversible) oxidative deamination of glutamate to α-ketoglutarate accompanied by a reduction of NAD+ to NADH. GDH connects amino acid, carbohydrate, neurotransmitter and oxidative energy metabolism. Glutamine is a neurotransmitter precursor used by neurons to sustain the pool of glutamate, but glutamine is also vividly oxidized for support of energy metabolism. This study investigates the role of GDH in neuronal metabolism by employing the Cns- Glud1−/− mouse, lacking GDH in the brain (GDH KO) and metabolic mapping using 13C-labelled glutamine and glucose. We observed a severely reduced oxidative glutamine metabolism during glucose deprivation in synaptosomes and cultured neurons not expressing GDH. In contrast, in the presence of glucose, glutamine metabolism was not affected by the lack of GDH expression. Respiration fuelled by glutamate was significantly lower in brain mitochondria from GDH KO mice and synaptosomes were not able to increase their respiration upon an elevated energy demand. The role of GDH for metabolism of glutamine and the respiratory capacity underscore the importance of GDH for neurons particularly during an elevated energy demand, and it may reflect the large allosteric activation of GDH by ADP.

The use of siRNA as a pharmacological tool to assess a role for the transcription factor NF-IL6 in the brain under in vitro and in vivo conditions during LPS-induced inflammatory stimulation

2017 ◽  
Vol 28 (6) ◽  
Author(s):  
Jelena Damm ◽  
Joachim Roth ◽  
Rüdiger Gerstberger ◽  
Christoph Rummel
Keyword(s):  
Transcription Factor ◽  
Brain Cells ◽  
Nuclear Factor ◽  
Si Rna ◽  
The Brain ◽  
Deficient Mice ◽  
Transcription Factor Nuclear Factor

AbstractBackground:Studies with NF-IL6-deficient mice indicate that this transcription factor plays a dual role during systemic inflammation with pro- and anti-inflammatory capacities. Here, we aimed to characterize the role of NF-IL6 specifically within the brain.Methods:In this study, we tested the capacity of short interfering (si) RNA to silence the inflammatory transcription factor nuclear factor-interleukin 6 (NF-IL6) in brain cells underResults:In cells of a mixed neuronal and glial primary culture from the ratConclusions:This approach was, thus, not suitable to characterize the role NF-IL6 in the brain

scholarly journals Is There a Link between Oropharyngeal Microbiome and Schizophrenia? A Narrative Review

2022 ◽  
Vol 23 (2) ◽  
pp. 846
Author(s):  
Stanislas Martin ◽  
Audrey Foulon ◽  
Wissam El Hage ◽  
Diane Dufour-Rainfray ◽  
Frédéric Denis
Keyword(s):  
Periodontal Disease ◽  
Research Team ◽  
Oral Microbiome ◽  
Oral Microbiota ◽  
Future Studies ◽  
The Subject ◽  
The Moment ◽  
The Impact ◽  
The Brain

The study aimed to examine the impact of the oropharyngeal microbiome in the pathophysiology of schizophrenia and to clarify whether there might be a bidirectional link between the oral microbiota and the brain in a context of dysbiosis-related neuroinflammation. We selected nine articles including three systemic reviews with several articles from the same research team. Different themes emerged, which we grouped into 5 distinct parts concerning the oropharyngeal phageome, the oropharyngeal microbiome, the salivary microbiome and periodontal disease potentially associated with schizophrenia, and the impact of drugs on the microbiome and schizophrenia. We pointed out the presence of phageoma in patients suffering from schizophrenia and that periodontal disease reinforces the role of inflammation in the pathophysiology of schizophrenia. Moreover, saliva could be an interesting substrate to characterize the different stages of schizophrenia. However, the few studies we have on the subject are limited in scope, and some of them are the work of a single team. At this stage of knowledge, it is difficult to conclude on the existence of a bidirectional link between the brain and the oral microbiome. Future studies on the subject will clarify these questions that for the moment remain unresolved.

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.

Drugs and Drug Policy

2011 ◽  
Author(s):  
Mark A.R. Kleiman ◽  
Jonathan P. Caulkins ◽  
Angela Hawken
Keyword(s):  
Drug Policy ◽  
Illicit Trade ◽  
Beneficial Effects ◽  
Control Drug ◽  
The Subject ◽  
Drugs And Crime ◽  
The Relationship ◽  
Drug Free ◽  
The Brain

While there have always been norms and customs around the use of drugs, explicit public policies--regulations, taxes, and prohibitions--designed to control drug abuse are a more recent phenomenon. Those policies sometimes have terrible side-effects: most prominently the development of criminal enterprises dealing in forbidden (or untaxed) drugs and the use of the profits of drug-dealing to finance insurgency and terrorism. Neither a drug-free world nor a world of free drugs seems to be on offer, leaving citizens and officials to face the age-old problem: What are we going to do about drugs? In Drugs and Drug Policy, three noted authorities survey the subject with exceptional clarity, in this addition to the acclaimed series, What Everyone Needs to Know. They begin by, defining "drugs, " examining how they work in the brain, discussing the nature of addiction, and exploring the damage they do to users. The book moves on to policy, answering questions about legalization, the role of criminal prohibitions, and the relative legal tolerance for alcohol and tobacco. The authors then dissect the illicit trade, from street dealers to the flow of money to the effect of catching kingpins, and show the precise nature of the relationship between drugs and crime. They examine treatment, both its effectiveness and the role of public policy, and discuss the beneficial effects of some abusable substances. Finally they move outward to look at the role of drugs in our foreign policy, their relationship to terrorism, and the ugly politics that surround the issue. Crisp, clear, and comprehensive, this is a handy and up-to-date overview of one of the most pressing topics in today's world.

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.

A Microscopic Demonstration of the Normal and Pathological Histology of Mesoglia Cells

1900 ◽  
Vol 46 (195) ◽  
pp. 724-724 ◽  
Author(s):  
Ford Robertson
Keyword(s):  
Cell Body ◽  
Brain Structure ◽  
Grey Matter ◽  
Brain Cells ◽  
Nerve Fibres ◽  
Pathological Conditions ◽  
Exact Function ◽  
Microscopic Demonstration ◽  
A Cell ◽  
The Brain

Dr. Clouston in the unavoidable absence of Dr. Ford Robertson made the following remarks:—The first fact that I have to direct the attention of the meeting to is that Dr. Ford Robertson has devised a new method of examining nerve-tissues by depositing platinum in them. By the use of this platinum method he has demonstrated, amongst other things, that what is called the neuroglia is composed of two sets of elements instead of one, as is generally considered. The neuroglia, as exhibited by this and other methods, is attached to the arteries, to the fibres, and to the brain-cells, forming a generally supporting medium. Dr. Robertson has discovered that in addition to this there is another set of cells, which he has called the mesoglia cells, consisting in a typical form of a cell-body, a nucleus and a number of processes. These processes are in no way connected either with the vascular substance or with the nerve-cells or the nerve-fibres. The mesoglia cells are entirely different from neuroglia cells in appearance, and are found in both the white and grey matter, and in such abundance that Dr. Robertson thinks that there are as many mesoglia cells as there are neuroglia cells existing all through the brain. Sometimes they have no processes, sometimes two processes, but the illustrations show a typical mesoglia cell from the dog and from man. The exact function of these mesoglia cells we certainly do not know, but they certainly do not act in any way as a support to the general brain structure. The mesoglia cells seem to have a phagocyte action in certain pathological conditions. They supply, if not all, at least the greater part of the amyloid bodies which are found in some of the chronic brain degenerations. I think you will agree that it is very important that Dr. Ford Robertson should have discovered a new element in the brain, the particular use of which will doubtless be demonstrated by some of the large number of enthusiastic workers on this subject.

scholarly journals The role of astroglia in neuroprotection

2009 ◽  
Vol 11 (3) ◽  
pp. 281-295 ◽  
Keyword(s):  
Oxidative Stress ◽  
Hepatic Encephalopathy ◽  
Energy Metabolism ◽  
Defense Mechanisms ◽  
Ion Homeostasis ◽  
Cell Type ◽  
Pathological Conditions ◽  
Constant Support ◽  
Brain Homeostasis

Astrocytes are the main neural cell type responsible for the maintenance of brain homeostasis. They form highly organized anatomical domains that are interconnected into extensive networks. These features, along with the expression of a wide array of receptors, transporters, and ion channels, ideally position them to sense and dynamically modulate neuronal activity. Astrocytes cooperate with neurons on several levels, including neurotransmitter trafficking and recycling, ion homeostasis, energy metabolism, and defense against oxidative stress. The critical dependence of neurons upon their constant support confers astrocytes with intrinsic neuroprotective properties which are discussed here. Conversely, pathogenic stimuli may disturb astrocytic function, thus compromising neuronal functionality and viability. Using neuroinflammation, Alzheimer's disease, and hepatic encephalopathy as examples, we discuss how astrocytic defense mechanisms may be overwhelmed in pathological conditions, contributing to disease progression.

scholarly journals Gut and Brain: Investigating Physiological and Pathological Interactions Between Microbiota and Brain to Gain New Therapeutic Avenues for Brain Diseases

2021 ◽  
Vol 15 ◽  
Author(s):  
Gabriele Deidda ◽  
Manuele Biazzo
Keyword(s):  
Gut Microbiota ◽  
Therapeutic Strategy ◽  
Brain Diseases ◽  
Microbial Populations ◽  
Normal Brain ◽  
Neuronal Populations ◽  
Brain Physiology ◽  
Pathological Conditions ◽  
The Brain

Brain physiological functions or pathological dysfunctions do surely depend on the activity of both neuronal and non-neuronal populations. Nevertheless, over the last decades, compelling and fast accumulating evidence showed that the brain is not alone. Indeed, the so-called “gut brain,” composed of the microbial populations living in the gut, forms a symbiotic superorganism weighing as the human brain and strongly communicating with the latter via the gut–brain axis. The gut brain does exert a control on brain (dys)functions and it will eventually become a promising valuable therapeutic target for a number of brain pathologies. In the present review, we will first describe the role of gut microbiota in normal brain physiology from neurodevelopment till adulthood, and thereafter we will discuss evidence from the literature showing how gut microbiota alterations are a signature in a number of brain pathologies ranging from neurodevelopmental to neurodegenerative disorders, and how pre/probiotic supplement interventions aimed to correct the altered dysbiosis in pathological conditions may represent a valuable future therapeutic strategy.

scholarly journals The Role of GPNMB in Inflammation

2021 ◽  
Vol 12 ◽  
Author(s):  
Marina Saade ◽  
Giovanna Araujo de Souza ◽  
Cristoforo Scavone ◽  
Paula Fernanda Kinoshita
Keyword(s):  
Neurodegenerative Diseases ◽  
Innate Immune ◽  
Inflammatory Conditions ◽  
Pathological Conditions ◽  
Published Evidence ◽  
The Central Nervous System ◽  
Inflammation Resolution ◽  
The Brain ◽  
Lps Treatment

Inflammation is a response to a lesion in the tissue or infection. This process occurs in a specific manner in the central nervous system and is called neuroinflammation, which is involved in neurodegenerative diseases. GPNMB, an endogenous glycoprotein, has been recently related to inflammation and neuroinflammation. GPNMB is highly expressed in macrophages and microglia, which are cells involved with innate immune response in the periphery and the brain, respectively. Some studies have shown increased levels of GPNMB in pro-inflammatory conditions, such as LPS treatment, and in pathological conditions, such as neurodegenerative diseases and cancer. However, the role of GPNMB in inflammation is still not clear. Even though most studies suggest that GPNMB might have an anti-inflammatory role by promoting inflammation resolution, there is evidence that GPNMB could be pro-inflammatory. In this review, we gather and discuss the published evidence regarding this interaction.

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