Results 161 to 170 of about 79,124 (218)
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Excitotoxicity and mitochondria
Biochemical Society Symposia, 1999Excitotoxicity is the process whereby a massive glutamate release in the central nervous system in response to ischaemia or related trauma leads to the delayed, predominantly necrotic death of neurons. Excitotoxicity is also implicated in a variety of slow neurodegenerative disorders.
D G, Nicholls +3 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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Neurology, 1996
This review will summarize current understanding of the molecular and cellular mechanisms of excitotoxicity, the organization of glutamate systems in relation to ALS and evidence that excitotoxicity is relevant to the pathogenesis of ALS.
P N, Leigh, B S, Meldrum
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This review will summarize current understanding of the molecular and cellular mechanisms of excitotoxicity, the organization of glutamate systems in relation to ALS and evidence that excitotoxicity is relevant to the pathogenesis of ALS.
P N, Leigh, B S, Meldrum
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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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Journal of Neurobiology, 1992
AbstractExcitotoxicity refers to the ability of glutamate or related excitatory amino acids to mediate the death of central neurons under certain conditions, for example, after intense exposure. Such excitotoxic neuronal death may contribute to the pathogenesis of brain or spinal cord injury associated with several human disease states.
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AbstractExcitotoxicity refers to the ability of glutamate or related excitatory amino acids to mediate the death of central neurons under certain conditions, for example, after intense exposure. Such excitotoxic neuronal death may contribute to the pathogenesis of brain or spinal cord injury associated with several human disease states.
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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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