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Excitotoxicity and neurodegenerative diseases
Current Opinion in Neurology, 1995Glutamate is an excitatory neurotransmitter in the mammalian central nervous system and a neurotoxin (excitotoxin) that has the potential to destroy neurones by activation of ionotropic receptors. In contrast to the well documented role of glutamate in the pathogenesis of neuronal degeneration resulting from hypoxia/ischaemia, hypoglycaemia, status ...
C, Ikonomidou, L, Turski
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Pathophysiology of oligodendroglial excitotoxicity
Journal of Neuroscience Research, 1996Oligodendrocyte-like cells (OLD) derived from the rat oligodendroglial precursor line, CG-4, express Ca(2+)-permeable non-methyl-D-aspartate glutamate receptor channels (GluR). Exposure to kainate, an L-glutamate analogue, markedly elevates OLC Ca2+ influx and cytosolic [Ca2+], and results in damage to both OLC plasma membrane and OLC nuclear DNA.
A, Yoshioka, B, Bacskai, D, Pleasure
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European Journal of Pharmacology, 2002
Excitotoxicity results from prolonged activation of glutamate receptors expressed by cells in the central nervous system (CNS). This cell death mechanism was first discovered in retinal ganglion cells and subsequently in brain neurons. In addition, it has been recently observed that CNS glial cells can also undergo excitotoxicity.
Carlos, Matute +3 more
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Excitotoxicity results from prolonged activation of glutamate receptors expressed by cells in the central nervous system (CNS). This cell death mechanism was first discovered in retinal ganglion cells and subsequently in brain neurons. In addition, it has been recently observed that CNS glial cells can also undergo excitotoxicity.
Carlos, Matute +3 more
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Apoptosis, Excitotoxicity, and Neuropathology
Experimental Cell Research, 1998While a high rate of cell loss is tolerated and even required to model the developing nervous system, an increased rate of cell death in the adult nervous system underlies neurodegenerative disease. Evolutionarily conserved mechanisms involving proteases, Bcl-2-related proteins, p53, and mitochondrial factors participate in the modulation and execution
M, Leist, P, Nicotera
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Calcium, ischemia and excitotoxicity
Cell Calcium, 2010The initial reports regarding a cytotoxic role of calcium ions were published over 30 years ago. In neurons, calcium ions can gain entry into the cell through several mechanisms. These include the over-activation of glutamate receptors (NMDA, AMPA, KA) or of a range of channels and transporters (TRPM2, TRPM7, NCX, ASICs, CaV1.2, and hemichannels ...
Kinga, Szydlowska, Michael, Tymianski
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Excitotoxicity in neonatal hypoxia
Mental Retardation and Developmental Disabilities Research Reviews, 2001AbstractHypoxic‐ischemic encephalopathy (HIE) in neonates is a disorder of excessive neuronal excitation that includes seizures, abnormal EEG activity, and delayed failure of oxidative metabolism with elevated levels of lactic acid in the brain. Evidence from experimental models and clinical investigation indicates that HIE is triggered by a profound ...
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TRP Channels in Excitotoxicity
The NeuroscientistGlutamate excitotoxicity is a central mechanism contributing to cellular dysfunction and death in various neurological disorders and diseases, such as stroke, traumatic brain injury, epilepsy, schizophrenia, addiction, mood disorders, Huntington’s disease, Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, pathologic pain, and even normal ...
Pengyu Zong +3 more
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1998
Excitotoxins are a special group of neurotoxic substances that excite somatic and dendritic receptors in such a way that the neurons may die. All excitotoxins are in principle agonists of glutamate receptors in the brain and are structurally related to glutamate.
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Excitotoxins are a special group of neurotoxic substances that excite somatic and dendritic receptors in such a way that the neurons may die. All excitotoxins are in principle agonists of glutamate receptors in the brain and are structurally related to glutamate.
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Wernicke’s encephalopathy: an excitotoxicity hypothesis
Metabolic Brain Disease, 1997Thiamine deficiency is a recognized cause of Wernicke's encephalopathy (WE), a condition in which small necrotic lesions are found in close proximity to the third and fourth ventricles and the Sylvian aqueduct. Although the neuropathology of WE is well-established, the pathogenic mechanisms that determine the formation and distribution of brain lesions
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