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Excitotoxicity in glial cells

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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Apoptosis, Excitotoxicity, and Neuropathology

Experimental Cell Research, 1998
While 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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Excitotoxicity

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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Calcium, ischemia and excitotoxicity

Cell Calcium, 2010
The 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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Excitotoxic cell death

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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Excitotoxicity in Aging and Dementia

1983
The extracellular concentration of glutamate in the neocortex of human brain may-increase progressively with ageing. Glutamergic nerve terminals seem to be a major source of the amino acid. There is no evidence that the concentration of extracellular glutamate is increased in the neocortex in Alzheimer’s disease.
D. M. Bowen   +2 more
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EXCITOTOXICITY AS A STOCHASTIC PROCESS

Clinical and Experimental Pharmacology and Physiology, 1995
SUMMARY1. Neuronal death following excitotoxic insult appears to be a stochastic process involving transition through an intermediate biochemical state.2. Hydrogen ion accumulation in the hours after toxic glutamate exposure may indicate that this transition has occurred.
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Excitotoxicity in neonatal hypoxia

Mental Retardation and Developmental Disabilities Research Reviews, 2001
AbstractHypoxic‐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 Neuroscientist
Glutamate 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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Excitotoxicity in Autism

2008
Autism spectrum disorders are neurodevelopmental disorders characterized by deficits in social skills, communication, and motor function, as well as compulsive and repetitive behaviors and interests. Although these disorders are thought to be of multifactorial origin, with a wide range of genetic and environmental factors implicated, we propose that ...
Martin Evers, Eric Hollander
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