scholarly journals Are glial cells involved in functional hyperemia in the brain?

2014 ◽  
Vol 143 (6) ◽  
pp. 314-314
Author(s):  
Yohei Okubo
Keyword(s):  
Glial Cells ◽  
Functional Hyperemia ◽  
The Brain

scholarly journals The Microbiota–Gut–Brain Axis and Alzheimer Disease. From Dysbiosis to Neurodegeneration: Focus on the Central Nervous System Glial Cells

2021 ◽  
Vol 10 (11) ◽  
pp. 2358
Author(s):  
Maria Grazia Giovannini ◽  
Daniele Lana ◽  
Chiara Traini ◽  
Maria Giuliana Vannucchi
Keyword(s):  
Alzheimer Disease ◽  
Glial Cells ◽  
Cell Types ◽  
The Past ◽  
The Central Nervous System ◽  
Diseased State ◽  
The Brain ◽  
Alzheimer Disease Pathogenesis ◽  
Brain Homeostasis

The microbiota–gut system can be thought of as a single unit that interacts with the brain via the “two-way” microbiota–gut–brain axis. Through this axis, a constant interplay mediated by the several products originating from the microbiota guarantees the physiological development and shaping of the gut and the brain. In the present review will be described the modalities through which the microbiota and gut control each other, and the main microbiota products conditioning both local and brain homeostasis. Much evidence has accumulated over the past decade in favor of a significant association between dysbiosis, neuroinflammation and neurodegeneration. Presently, the pathogenetic mechanisms triggered by molecules produced by the altered microbiota, also responsible for the onset and evolution of Alzheimer disease, will be described. Our attention will be focused on the role of astrocytes and microglia. Numerous studies have progressively demonstrated how these glial cells are important to ensure an adequate environment for neuronal activity in healthy conditions. Furthermore, it is becoming evident how both cell types can mediate the onset of neuroinflammation and lead to neurodegeneration when subjected to pathological stimuli. Based on this information, the role of the major microbiota products in shifting the activation profiles of astrocytes and microglia from a healthy to a diseased state will be discussed, focusing on Alzheimer disease pathogenesis.

scholarly journals Neuron–Glia Interactions in Tuberous Sclerosis Complex Affect the Synaptic Balance in 2D and Organoid Cultures

Cells ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 134
Author(s):  
Stephanie Dooves ◽  
Arianne J. H. van Velthoven ◽  
Linda G. Suciati ◽  
Vivi M. Heine
Keyword(s):  
Tuberous Sclerosis ◽  
Glial Cells ◽  
Tuberous Sclerosis Complex ◽  
Neuronal Development ◽  
Transmembrane Proteins ◽  
Significant Burden ◽  
Epidermal Growth ◽  
And Control ◽  
Egf Signaling ◽  
The Brain

Tuberous sclerosis complex (TSC) is a genetic disease affecting the brain. Neurological symptoms like epilepsy and neurodevelopmental issues cause a significant burden on patients. Both neurons and glial cells are affected by TSC mutations. Previous studies have shown changes in the excitation/inhibition balance (E/I balance) in TSC. Astrocytes are known to be important for neuronal development, and astrocytic dysfunction can cause changes in the E/I balance. We hypothesized that astrocytes affect the synaptic balance in TSC. TSC patient-derived stem cells were differentiated into astrocytes, which showed increased proliferation compared to control astrocytes. RNA sequencing revealed changes in gene expression, which were related to epidermal growth factor (EGF) signaling and enriched for genes that coded for secreted or transmembrane proteins. Control neurons were cultured in astrocyte-conditioned medium (ACM) of TSC and control astrocytes. After culture in TSC ACM, neurons showed an altered synaptic balance, with an increase in the percentage of VGAT+ synapses. These findings were confirmed in organoids, presenting a spontaneous 3D organization of neurons and glial cells. To conclude, this study shows that TSC astrocytes are affected and secrete factors that alter the synaptic balance. As an altered E/I balance may underlie many of the neurological TSC symptoms, astrocytes may provide new therapeutic targets.

THE METABOLISM OF NORMAL BRAIN AND HUMAN GLIOMAS IN RELATION TO CELL TYPE AND DENSITY

1955 ◽  
Vol 33 (3) ◽  
pp. 395-403 ◽  
Author(s):  
Irving H. Heller ◽  
K. A. C. Elliott
Keyword(s):  
Cerebral Cortex ◽  
White Matter ◽  
Brain Tumors ◽  
Corpus Callosum ◽  
Oxygen Uptake ◽  
Glial Cells ◽  
Cerebellar Cortex ◽  
Unit Weight ◽  
Uptake Rates ◽  
The Brain

Per unit weight, cerebral and cerebellar cortex respire much more actively than corpus callosum. The rate per cell nucleus is highest in cerebral cortex, lower in corpus callosum, and still lower in cerebellar cortex. The oxygen uptake rates of the brain tumors studied, with the exception of an oligodendroglioma, were about the same as that of white matter on the weight basis but lower than that of cerebral cortex or white matter on the cell basis. In agreement with previous work, an oligodendroglioma respired much more actively than the other tumors. The rates of glycolysis of the brain tumors per unit weight were low but, relative to their respiration rate, glycolysis was higher than in normal gray or white matter. Consideration of the figures obtained leads to the following tentative conclusions: Glial cells of corpus callosum respire more actively than the neurons of the cerebellar cortex. Neurons of the cerebral cortex respire on the average much more actively than neurons of the cerebellar cortex or glial cells. Considerably more than 70% of the oxygen uptake by cerebral cortex is due to neurons. The oxygen uptake rates of normal oligodendroglia and astrocytes are probably about the same as the rates found per nucleus in an oligodendroglioma and in astrocytomas; oligodendroglia respire much more actively than astrocytes.

scholarly journals Temporal gliosarcoma: case report and review of literature

2015 ◽  
Vol 22 (1) ◽  
pp. 112-116
Author(s):  
Amit Agrawal ◽  
Vissa Shanthi ◽  
Baddukonda Appala Ramakrishna ◽  
Kuppili Venkata Murali Mohan
Keyword(s):  
Case Report ◽  
Median Survival ◽  
Glial Cells ◽  
Primary Tumor ◽  
Clinical Presentation ◽  
Spindle Cell ◽  
Review Of Literature ◽  
Future Studies ◽  
Aggressive Tumor ◽  
The Brain

Abstract First characterized by Stroebe, the gliosarcomas are highly malignant and rare primary tumor of the brain composed of neoplastic glial cells in association with spindle cell sarcomatous elements (biphasic tissue patterns). In spite of being recognized as two different pathologies studies have not shown any significant differences between gliosarcoma and glioblastoma with regard to age, sex, size, clinical presentation, and median survival. In summary, gliosarcoma is an aggressive tumor with a propensity to recur and re-grow with poor outcome. Future studies are needed to understand the true pathology of these biphasic tumors.

The brain-specific protein MLC1 implicated in megalencephalic leukoencephalopathy with subcortical cysts is expressed in glial cells in the murine brain

Glia ◽  
2003 ◽  
Vol 44 (3) ◽  
pp. 283-295 ◽  
Author(s):  
Angelika Schmitt ◽  
Viktor Gofferje ◽  
Melanie Weber ◽  
Jobst Meyer ◽  
Rainald Mössner ◽  
...  
Keyword(s):  
Glial Cells ◽  
Specific Protein ◽  
Murine Brain ◽  
The Brain ◽  
Subcortical Cysts

scholarly journals Effects of cadmium on the glial architecture in lizard brain

2017 ◽  
Author(s):  
Rossana Favorito ◽  
Antonio Monaco ◽  
Maria C. Grimaldi ◽  
Ida Ferrandino
Keyword(s):  
Blood Brain Barrier ◽  
Glial Cells ◽  
Toxic Metal ◽  
Chemical Exposure ◽  
Brain Barrier ◽  
Cresyl Violet ◽  
Cytotoxic Action ◽  
Morphological Alterations ◽  
Blood Brain ◽  
The Brain

The glial cells are positioned to be the first cells of the brain parenchyma to face molecules crossing the blood-brain barrier with a relevant neuroprotective role from cytotoxic action of heavy metals on the nervous system. Cadmium is a highly toxic metal and its levels in the environment are increasing due to industrial activities. This element can pass the blood-brain barrier and have neurotoxic activity. For this reason we have studied the effects of cadmium on the glial architecture in the lizard Podarcis siculus, a significant bioindicator of chemical exposure due to its persistence in a variety of habitats. The study was performed on two groups of lizards. The first group of P. siculus was exposed to an acute treatment by a single i.p. injection (2 mg/kg-BW) of CdCl2 and sacrificed after 2, 7 and 16 days. The second one was used as control. The histology of the brain was studied by Hematoxylin/Eosin and Cresyl/Violet stains while the glial structures were analyzed by immunodetection of the glial fibrillary acidic protein (GFAP), the most widely accepted marker for astroglial cells. Evident morphological alterations of the brain were observed at 7 and 16 days from the injection, when we revealed also a decrease of the GFAP-immunopositive structures in particular in the rhombencephalic ventricle, telencephalon and optic tectum. These results show that in the lizards an acute exposure to cadmium provokes morphological cellular alterations in the brain but also a decrement of the expression of GFAP marker with possible consequent damage of glial cells functions.

scholarly journals Pathological potential of astroglia

2008 ◽  
pp. S101-S110
Author(s):  
A Chvátal ◽  
M Anděrová ◽  
H Neprašová ◽  
I Prajerová ◽  
J Benešová ◽  
...  
Keyword(s):  
Glial Cells ◽  
Brain Parenchyma ◽  
Brain Diseases ◽  
Brain Pathology ◽  
Pathological Conditions ◽  
Recent Developments ◽  
Neurological Defect ◽  
Del Rio ◽  
The Brain ◽  
Brain Homeostasis

The pathological potential of glial cells was recognized already by Rudolf Virchow, Santiago Ramon y Cajal and Pio Del Rio-Ortega. Many functions and roles performed by astroglia in the healthy brain determine their involvement in brain diseases; as indeed any kind of brain insult does affect astrocytes, and their performance in pathological conditions, to a very large extent, determines the survival of the brain parenchyma, the degree of damage and neurological defect. Astrocytes being in general responsible for overall brain homeostasis are involved in virtually every form of brain pathology. Here we provide an overview of recent developments in identifying the role and mechanisms of the pathological potential of astroglia.

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 Universal Glia to Neurone Lactate Transfer in the Nervous System: Physiological Functions and Pathological Consequences

Biosensors ◽  
2020 ◽  
Vol 10 (11) ◽  
pp. 183 ◽  
Author(s):  
Carolyn L. Powell ◽  
Anna R. Davidson ◽  
Angus M. Brown
Keyword(s):  
Glial Cells ◽  
Lactate Production ◽  
Extracellular Fluid ◽  
Pathological Conditions ◽  
Motor End Plate ◽  
Lactate Uptake ◽  
The Brain ◽  
Intense Debate ◽  
Lateral Sclerosis ◽  
Glucose Availability

Whilst it is universally accepted that the energy support of the brain is glucose, the form in which the glucose is taken up by neurones is the topic of intense debate. In the last few decades, the concept of lactate shuttling between glial elements and neural elements has emerged in which the glial cells glycolytically metabolise glucose/glycogen to lactate, which is shuttled to the neural elements via the extracellular fluid. The process occurs during periods of compromised glucose availability where glycogen stored in astrocytes provides lactate to the neurones, and is an integral part of the formation of learning and memory where the energy intensive process of learning requires neuronal lactate uptake provided by astrocytes. More recently sleep, myelination and motor end plate integrity have been shown to involve lactate shuttling. The sequential aspect of lactate production in the astrocyte followed by transport to the neurones is vulnerable to interruption and it is reported that such disparate pathological conditions as Alzheimer’s disease, amyotrophic lateral sclerosis, depression and schizophrenia show disrupted lactate signalling between glial cells and neurones.

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