Ischemia-Triggered Glutamate Excitotoxicity From the Perspective of Glial Cells

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...

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Vydané v:	Frontiers in cellular neuroscience Ročník 14; s. 51
Hlavní autori:	Belov Kirdajova, Denisa, Kriska, Jan, Tureckova, Jana, Anderova, Miroslava
Médium:	Journal Article
Jazyk:	English
Vydavateľské údaje:	Switzerland Frontiers Research Foundation 19.03.2020 Frontiers Media S.A
Predmet:	Amino acids Apoptosis Astrocytes Calcium (extracellular) Calcium (intracellular) Cell death Cell membranes Cellular Neuroscience Central nervous system Cerebral blood flow Depolarization Edema Excitotoxicity Free radicals Gene expression Glial cells glutamate excitotoxicity glutamate uptake/release Glutamic acid receptors Ischemia ischemic pathway Membrane potential Metabolism Metabolites Microglia Mortality Neurological diseases Neuronal-glial interactions Oligodendrocytes Oxidative phosphorylation Parenchyma Phosphorylation Physiology glutamate excitotoxicity ischemic pathway cell death glutamate uptake/release oligodendrocytes astrocytes NG2 glia glutamate receptors and transporters
ISSN:	1662-5102, 1662-5102
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Popis
Shrnutí:	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 (Ca ) 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 Ca ions and aberrant glutamate release, aggravating the effect of this ischemic pathway. The activation of downstream Ca -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.
Bibliografia:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Edited by: Balázs Pál, University of Debrecen, Hungary Reviewed by: Yuriy Pankratov, University of Warwick, United Kingdom; Mario Valentino, University of Malta, Malta
ISSN:	1662-5102 1662-5102
DOI:	10.3389/fncel.2020.00051