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Topic: Excitotoxicity

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	Excitotoxicity - Wikipedia, the free encyclopedia
		Excitotoxicity is the pathological process by which neurons are damaged and killed by the overactivations of receptors for the excitatory neurotransmitter glutamate, such as the NMDA receptor and AMPA receptor.
		Ischemia is followed by accumulation of glutamate and aspartate in the extracellular fluid, causing cell death, which is aggravated by lack of oxygen and glucose.
		The biochemical cascade resulting from ischemia and involving excitotoxicity is called the ischemic cascade.
	en.wikipedia.org /wiki/Excitotoxicity (999 words)

	[No title]
		Named in 1969 by Dr. John Olney, excitotoxicity is a phenomenon characterized by the triggering of neuronal excitation through over-stimulation of susceptible neurons by the excitatory amino acids, primarily glutamate and aspartate.
		There is considerable evidence that excitotoxicity is responsible for much of the pathological damage produced by prolonged seizures.30,31 This destructive process has been proposed as the mechanism for both the mirror focus seen with temporal lobe seizures and the cognitive deterioration associated with status epilepiticus.
		Excitotoxicity is intimately connected to seizures and explains the neural damage seen when they are prolonged or repeated.
	www.dorway.com /blayautism.txt (6430 words)

	INABIS '98 - Motoneuron Diseases,Excitotoxicity and Oxidative Stress
		In the recent years, the relations between excitotoxicity and oxidative stress were discovered suggesting that these combined mechanisms of neuronal death could both contribute to neuronal loss detected in several neurological disorders.
		Excitotoxicity was implicated in a large variety of neurological disorder (4) including motoneuron diseases.
		The combination of excitotoxicity and free radicals toxicity could be at the origin of a selective motoneuron death in ALS.
	www.mcmaster.ca /inabis98/juurlink/hugon0510/two.html (1553 words)

	Excitotoxicity and Neuroprotection/Brainstorms June 1997 (Site not responding. Last check: 2007-11-03)
		It is possible that the brain needs this excitotoxic mechanism so that glutamate can act as a gardener in the brain, pruning worn out branches from dendrite trees so that healthy new sprouts might prosper.
		At an extreme, glutamate is a mass murderer, wreaking the destruction of localized neurons during the chaos of stroke.
		Another approach to developing treatments for illnesses that may be mediated by excitotoxicity is to rescue the cellular machinery once glutamate's cascade of doom has been activated.
	www.psychiatrist.com /pcc/brainstorm/br5806.htm (727 words)

	Sound and Fury Article
		In the face of this connection between excitotoxicity and the pathophysiology of MS, it would be ludicrous to allow further use of this excitotoxin containing sweetener..
		Excitotoxic insults to the optic nerve alter visual evoked potentials.
		Chronic microglial activation and excitotoxicity secondary to excessive immune stimulation: possible factors in Gulf War Syndrome and autism.
	www.soundandfury.tv /pages/article.html (950 words)

	Excitotoxicity: Perspectives Based on N-Methyl-D-Aspartate Receptor Subtypes -- Lynch and Guttmann 300 (3): 717 -- ...
		Pizzi M, Boroni F, Bianchetti KM, Memo M and Spano P (1999) Reversal of glutamate excitotoxicity by activation of PKC-associated metabotropic glutamate receptors in cerebellar granule cells relies on NR2C subunit expression.
		Standaert DG, Landwehrmeyer GB, Kerner JA, Jr, Penney JB and Young AB (1996) Expression of NMDAR2D glutamate receptor subunit mRNA in neurochemically identified interneurons in the rat neostriatum, neorcortex and hippocampus.
		Williams K, Russell SL, Shen YM and Molinoff PB (1993) Developmental switch in the expression of NMDA receptors occurs in vivo and in vitro.
	jpet.aspetjournals.org /cgi/content/full/300/3/717 (5157 words)

	Bates College \| 2001
		Excitotoxicity has been linked to brain damage caused by stroke and neurodegenerative disease such as Alzheimer's Disease and Parkinson's Syndrome.
		Excitotoxicity was induced in the lab with O.5mM glut application to neuronal forebrain cultures of E 19 Sprague-Dawley rats.
		The resultant excitotoxicity was combated using NMDA receptor antagonists (100uM APV) and non-NMDA receptor antagonists (10uM CNQX) that both produced neuroprotective trends, although not significant (n=5).
	www.bates.edu /x57973.xml (2325 words)

	HBHealth ~ What's New In Anti-Ageing
		Excitotoxic damage may occur to cortex or hippocampus neurons at levels around 2-5 micromoles/liter (3).
		The chronic forms of excitotoxic brain injury will usually occur much more slowly, and the effects may be subtle until the final stage of the damage.
		And the excitotoxic damage from excess GLU may take a lifetime to develop to the point of expressing itself as a stroke, Alzheimer's or Parkinson's disease, etc. But high dose GAM can cause excitotoxic problems even in the short term.
	www.hbhealthonline.com /whatsnew06.html (5918 words)

	Glutamate Toxicity (Site not responding. Last check: 2007-11-03)
		The role of excitotoxicity in neurodegenerative disease: implications for therapy.
		This process of neuronal death is called excitotoxicity and appears to involve sustained elevations of intracellular calcium levels.
		Much attention has been directed at obtaining evidence for a role for excitotoxicity in the neurological sequelae of stroke, and there now seems to be little doubt that such a process is indeed a determining factor in the extent of the lesions observed.
	www.altcorp.com /AffinityLaboratory/gsglutamate.htm (1258 words)

	Dietary Restriction
		These phenomena – impaired energy metabolism, oxidative stress, excitotoxicity, and apoptosis – are each believed to be somehow evoked by processes that the mutant huntingtin protein sets in motion.
		Glutamate is a neurotransmitter and is typically the culprit in excitotoxicity.
		As indicated by the fact that they are much more prevalent in nerve cells of mice with HD than mice without the disease, one of the key components in the apoptosis cascade in HD cells appears to be a group of proteins known as caspases.
	www.stanford.edu /group/hopes/treatmts/dietrestrict/dr3.html (1313 words)

	[No title]
		It is widely accepted that glutamate/Ca2+ excitotoxicity prominently contributes to acute neuronal necrosis against this background of varying energy supply and demand {Sattler, 2000 #2279; Choi, 1988 #816; Rothman, 1986 #455; Simon, 1984 #2420}.
		Hallmarks of glutamate/Ca2+ excitotoxicity are: (1) an excessive efflux of glutamate, (2) over-excitation of Ca2+-permeant, NMDA-subtype glutamatergic receptors and, subsequently, (3) elevated neuronal Ca2+ that overwhelms the regulatory capacity of the energy-deprived neuron {Sattler, 2000 #2279}{Choi, 1988 #816}{Rothman, 1986 #455}{Simon, 1984 #2420}.
		While the ischemic depolarization and its overt contribution to excitotoxic neuronal death have been well described, less is known about how electrophysiological events preceding the ischemic depolarization contribute to excitotoxicity.
	www.ttuhsc.edu /som/physiology/Fowler/IR_vs_AD_Manu_v20.doc (963 words)

	Causes and Consequences of Methamphetamine and MDMA Toxicity
		This process, termed excitotoxicity, is mediated by the activation of ionotropic and group 1 metabotropic glutamate receptors (iGluR and mGluR, respectively), leading to a rise in intracellular Ca levels.
		Taken together, these studies suggest that the mitochondria are common targets for the oxidative species and glutamate-mediated excitotoxicity produced by METH and MDMA, and that mitochondrial dysfunction and increased energy use play an important role in mediating the pro-oxidant and neurotoxic effects of the substituted amphetamines.
		Oxidative stress, excitotoxicity, and mitochondrial dysfunction appear to be causal events that converge to mediate METH and MDMA-induced neurotoxicity, as measured by loss of various markers of dopaminergic and serotonergic terminals (see Table 1 and diagram on Figure 5).
	www.aapsj.org /view.asp?art=aapsj080238 (6597 words)

	Glutamate Excitotoxicity Is Involved in Cell Death Caused by Tributyltin in Cultured Rat Cortical Neurons -- Nakatsu et ...
		Glutamate Excitotoxicity Is Involved in Cell Death Caused by Tributyltin in Cultured Rat Cortical Neurons -- Nakatsu et al.
		Glutamate Excitotoxicity Is Involved in Cell Death Caused by Tributyltin in Cultured Rat Cortical Neurons
		excitotoxicity caused by tributyltin is unrelated to apoptosis.
	toxsci.oxfordjournals.org /cgi/content/abstract/89/1/235 (281 words)

	Mutagenesis by environmental pollutants and biomonitoring of environmental mutagens
		Excitotoxicity is a mechanism commonly invoked to explain this.
		If glutamate-mediated excitotoxicity is to circumvent global damage and produce the regional pattern observed in AD, local modulation of cellular vulnerability is required.
		We discuss the experimental approaches that are required to elucidate excitotoxic mechanisms in a tissue in which glutamate is both the most abundant and ubiquitous excitatory transmitter, but also the most abundant and active intermediary metabolite.
	www.bentham.org /car/samples/car1-1/dodd/dodd-ms.htm (3666 words)

	How alcohol gives, and then takes away
		This damage -- a sensitization of the neurons to a process called excessive excitation or "excitotoxicity" through the N-methyl-D-aspartate (NMDA) glutamate receptor -- could be an important component in transitioning from experimentation to addiction.
		"This is one of the first studies to show a relationship between excitotoxicity, which likely occurs during ethanol withdrawal, and NMDA receptors," said Richard A. Morrisett, Associate Professor of Pharmacology at The University of Texas at Austin.
		Morrisett indicated there is a need for future studies that look at the effects of lower levels of alcohol on excitotoxicity.
	www.eurekalert.org /pub_releases/1999-11/ACER-Haga-131199.php (734 words)

	Pictorial Review of Glutamate Excitotoxicity: Fundamental Concepts for Neuroimaging -- Mark et al. 22 (10): 1813 -- ...
		Excitotoxicity induced by enhanced excitatory neurotransmission in cultured hippocampal pyramidal neurons.
		Glutamate excitotoxicity: a mechanism of neurologic injury associated with hypothermic circulatory arrest.
		Mitochondrial permeability transition (mPT) involvement in the neuronal excitotoxic pathway.
	www.ajnr.org /cgi/content/full/22/10/1813 (5169 words)

	The Influence of Glutamate Receptor 2 Expression on Excitotoxicity in GluR2 Null Mutant Mice -- Iihara et al. 21 (7): ...
		The Influence of Glutamate Receptor 2 Expression on Excitotoxicity in GluR2 Null Mutant Mice -- Iihara et al.
		The Influence of Glutamate Receptor 2 Expression on Excitotoxicity in GluR2 Null Mutant Mice
		excitotoxicity in the GluR2 mutant mice in vivo, because kainate
	www.jneurosci.org /cgi/content/full/21/7/2224 (6096 words)

	Excitotoxins - the ultimate brainslayer (Site not responding. Last check: 2007-11-03)
		Excitotoxins are biochemical substances (usually amino acids, amino acid analogs, or amino acid derivatives) that can react with specialized neuronal receptors - glutamate receptors - in the brain or spinal cord in such a way as to cause injury or death to a wide variety of neurons (1-3,8-10).
		And the excitotoxic damage from excess glutamate may take a lifetime to develop to the point of expressing itself as a stroke, Alzheimerâs or Parkinson's disease, etc. But high dose glutamine can cause excitotoxic problems even in the short term.
		A 1994 review article referred to excitotoxicity as "the final common pathway for neurologic disorders".(3) Yet public awareness of the excitotoxic phenomenon has been slow in coming, even in the life extension/natural medicine/health food communities.
	www.mysticalwonders.org /group/about1148.html (5817 words)

	Acetylcholine Protection of Adult Pig Retinal Ganglion Cells from Glutamate-Induced Excitotoxicity -- Wehrwein et al. ...
		Glutamate and glutamate agonists have excitotoxic effects on panned RGCs.
		-Bgt and MLA on the neuroprotective effect of nicotine on glutamate-induced excitotoxicity is demonstrated.
		Bar graphs demonstrate the effect of various concentration of choline on glutamate-induced excitotoxicity and the effect of 10 nM MLA on choline’s neuroprotection.
	www.iovs.org /cgi/content/full/45/5/1531 (7204 words)

	Role of metabotropic glutamate receptors in oligodendrocyte excitotoxicity and oxidative stress -- Deng et al. 101 ...
		Role of metabotropic glutamate receptors in oligodendrocyte excitotoxicity and oxidative stress -- Deng et al.
		Role of metabotropic glutamate receptors in oligodendrocyte excitotoxicity and oxidative stress
		excitotoxic OPC injury by inducing endocytosis of AMPA/kainate
	www.pnas.org /cgi/content/full/101/20/7751 (3690 words)

	Distinct Roles of Synaptic and Extrasynaptic NMDA Receptors in Excitotoxicity -- Sattler et al. 20 (1): 22 -- Journal ...
		Distinct Roles of Synaptic and Extrasynaptic NMDA Receptors in Excitotoxicity -- Sattler et al.
		Excitotoxic neuronal damage is the consequence of excessive stimulation of postsynaptic receptors by
		During an excitotoxic insult, presynaptically released glutamate binds to the NMDAR and induces Ca
	www.jneurosci.org /cgi/content/full/20/1/22 (7104 words)

	Regulation of proteins affecting NMDA receptor-induced excitotoxicity in a Huntington's mouse model -- Jarabek et al. ...
		Regulation of proteins affecting NMDA receptor-induced excitotoxicity in a Huntington's mouse model -- Jarabek et al.
		symptomatic N171-82Q mice to QA-induced excitotoxicity in the
		excitotoxicity is a contributing factor in secondary aspects
	brain.oxfordjournals.org /cgi/content/full/127/3/505 (6662 words)

	Nitric oxide mediates neurodegeneration and breakdown of the blood-brain barrier in tPA-dependent excitotoxic injury in ...
		Nitric oxide mediates neurodegeneration and breakdown of the blood-brain barrier in tPA-dependent excitotoxic injury in mice -- Parathath et al.
		Nitric oxide mediates neurodegeneration and breakdown of the blood-brain barrier in tPA-dependent excitotoxic injury in mice
		mice are resistant to KA-induced excitotoxicity, whereas wild-type mice are not.
	jcs.biologists.org /cgi/content/full/119/2/339 (6916 words)

	Complex Excitotoxicity In Neurodegenerative And Neuropsychiatric Disorders
		More recently we have expanded our focus to include "complex" excitotoxicity, a newly discovered phenomenon whereby blockade of Glu receptors on inhibitory neurons causes disinhibition of excitatory pathways leading to pathological release of excitotoxic activity from both cholinergic and glutamatergic neurons.
		We are examining the potential role of "complex" excitotoxicity in chronic neuropsychiatric disorders, such as schizophrenia and Alzheimer's disease.
		For example, excessive activation of Glu receptors triggers excitotoxic neurodegeneration, and insufficient activation of NMDA Glu receptors or excessive activation of GABA-A receptors triggers widespread apoptotic neurodegeneration.
	research.medicine.wustl.edu /ocfr/research.nsf/s/610FA6B82EA9E8FD8625677D005936EB (261 words)

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