Results 301 to 310 of about 80,747 (355)
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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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Microglia activation contributes to quinolinic acid-induced neuronal excitotoxicity through TNF-α
Apoptosis: an International Journal on Programmed Cell Death, 2017Zheng-Hong Qin, Qin Zheng-Hong
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Excitotoxicity in the Pathogenesis of Autism
Neurotoxicity Research, 2012Autism is a debilitating neurodevelopment disorder characterised by stereotyped interests and behaviours, and abnormalities in verbal and non-verbal communication. It is a multifactorial disorder resulting from interactions between genetic, environmental and immunological factors.
M M, Essa +4 more
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Alternative excitotoxic hypotheses
Neurology, 1992The concept of excitotoxicity, neuronal death produced by overstimulation of excitatory amino acid receptors, has become a popular way of explaining the pathogenesis of neuronal death in a variety of acute and chronic neurologic diseases. While there is strong evidence supporting the role of excitotoxicity in acute processes such as hypoxia/ischemia ...
R L, Albin, J T, Greenamyre
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Molecular Neurobiology, 1994
Neurochemical observations on cortical biopsies form 48 patients under surgical treatment for pharmacoresistant partial epilepsy showed a 70-80% increase in glutamate concentration when expressed in relation to neuron specific enolase. Intraperitoneal administration of one of its receptor agonists, kainic acid (KA), to the rat led to increased ...
K G, Haglid +3 more
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Neurochemical observations on cortical biopsies form 48 patients under surgical treatment for pharmacoresistant partial epilepsy showed a 70-80% increase in glutamate concentration when expressed in relation to neuron specific enolase. Intraperitoneal administration of one of its receptor agonists, kainic acid (KA), to the rat led to increased ...
K G, Haglid +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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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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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 Neuroscience, 2018
Traumatic brain injury (TBI) is a leading major cause of morbidity and mortality in youth and individuals under 45 year age. A wide variety of cellular and molecular mechanisms have been identified contributing to the pathogenesis of TBI.
Joel Tehse, C. Taghibiglou
semanticscholar +1 more source
Traumatic brain injury (TBI) is a leading major cause of morbidity and mortality in youth and individuals under 45 year age. A wide variety of cellular and molecular mechanisms have been identified contributing to the pathogenesis of TBI.
Joel Tehse, C. Taghibiglou
semanticscholar +1 more source
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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