Ischemia-Triggered Glutamate Excitotoxicity From the Perspective of Glial Cells
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378041%3A_____%2F20%3A00539601" target="_blank" >RIV/68378041:_____/20:00539601 - isvavai.cz</a>
Alternative codes found
RIV/00216208:11130/20:10410756
Result on the web
<a href="https://www.frontiersin.org/articles/10.3389/fncel.2020.00051/full" target="_blank" >https://www.frontiersin.org/articles/10.3389/fncel.2020.00051/full</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.3389/fncel.2020.00051" target="_blank" >10.3389/fncel.2020.00051</a>
Alternative languages
Result language
angličtina
Original language name
Ischemia-Triggered Glutamate Excitotoxicity From the Perspective of Glial Cells
Original language description
A plethora of neurological disorders shares a final common deadly pathway known as excitotoxicity. Among these disorders, ischemic injury is a prominent cause of death and disability worldwide. Brain ischemia stems from cardiac arrest or stroke, both responsible for insufficient blood supply to the brain parenchyma. Glucose and oxygen deficiency disrupts oxidative phosphorylation, which results in energy depletion and ionic imbalance, followed by cell membrane depolarization, calcium (Ca2+) overload, and extracellular accumulation of excitatory amino acid glutamate. If tight physiological regulation fails to clear the surplus of this neurotransmitter, subsequent prolonged activation of glutamate receptors forms a vicious circle between elevated concentrations of intracellular Ca2+ ions and aberrant glutamate release, aggravating the effect of this ischemic pathway. The activation of downstream Ca2+-dependent enzymes has a catastrophic impact on nervous tissue leading to cell death, accompanied by the formation of free radicals, edema, and inflammation. After decades of neuron-centric approaches, recent research has also finally shed some light on the role of glial cells in neurological diseases. It is becoming more and more evident that neurons and glia depend on each other. Neuronal cells, astrocytes, microglia, NG2 glia, and oligodendrocytes all have their roles in what is known as glutamate excitotoxicity. However, who is the main contributor to the ischemic pathway, and who is the unsuspecting victim? In this review article, we summarize the so-far-revealed roles of cells in the central nervous system, with particular attention to glial cells in ischemia-induced glutamate excitotoxicity, its origins, and consequences.
Czech name
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Czech description
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Classification
Type
J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database
CEP classification
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OECD FORD branch
30103 - Neurosciences (including psychophysiology)
Result continuities
Project
Result was created during the realization of more than one project. More information in the Projects tab.
Continuities
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Others
Publication year
2020
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Frontiers in Cellular Neuroscience
ISSN
1662-5102
e-ISSN
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Volume of the periodical
14
Issue of the periodical within the volume
mar.
Country of publishing house
CH - SWITZERLAND
Number of pages
27
Pages from-to
51
UT code for WoS article
000525584500001
EID of the result in the Scopus database
2-s2.0-85083254763