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Acute excitotoxicity

Sodium inflow and acute excitotoxicity. Neurotoxicity of excitatory amino acids is a direct consequence of the excessive excitatory depolarization—may be related to a loss of the ionic homeostasis and/or to a depletion of the energetic stocks of the cell (Olney et al. 1986). Neuronal damage could depend on the extracellular presence of sodium accompanied by a passive flow of chlorine and water (Hablitz and Langmoen 1982). Some considerations suggest that the acute excitatory swelling does not explain completely the damages induced by excitatory amino acids (Pulsinelli et al. 1982). [Pg.509]

Pang Z, Geddes JW (1997) Mechanisms of cell death induced by the mitochondrial toxin 3-nitropropionic acid acute excitotoxic necrosis and delayed apoptosis. J Neurosci 17 3064-3073 Papp MI, Kahn JE, Lantos PL (1989) Glial cytoplasmic inclusions in the CNS of patients with multiple system atrophy (striatonigral degeneration, olivopontocerebellar atrophy and Shy-Drager syndrome). J Neurol Sci 94 79-100... [Pg.95]

Berman, F.W., and Murray, TF 1999. Brevetoxins cause acute excitotoxicity in primary cultures of rat cerebellar granule neurons. Journal of Pharmacology and Experimental Therapeutics 290, 439-444. [Pg.44]

Polischuk, T.M., Jarvis, C.R., and Andrew, R.D., Intrinsic optical signaling denoting neuronal damage in response to acute excitotoxic insult by domoic acid in the hippocampal slice, Neurobiol. Dis., 4,423, 1998. [Pg.427]

Chapman GA, Moores K, Harrison D, Campbell CA, Stewart BR, Strijbos PJ (2000) Fractalkine cleavage from neuronal membranes represents an acute event in the inflammatory response to excitotoxic brain damage. J Neurosci 20 RC87... [Pg.186]

Budd, S. and Rao, T., Excitotoxicity in acute and chronic neurodegeneration, Curr. Opin. CPNS Investig. Drugs, 2, 403, 2000. [Pg.238]

Glutamate that is a major neurotransmitter in the mammalian nervous system not only plays a role in the development of the brain and learning but is also a potent neurotoxin when present in excess at synapses (Plaitakis and Shashidharan, 2000 Rausch et ah, 2006). Glutamate excitotoxicity has been shown to contribute to neuronal degeneration in acute conditions such as stroke, epilepsy, h) oglycemia, and chronic... [Pg.75]

Danysz W, Parsons CG, Mobius HJ, et al (2000) Neuroprotective and symptomatological action of memantine relevant for Alzheimer s disease—an unified glutamatergic hypothesis on the mechanism of action. Neurotox Res 2 85-97 Davis SM, Lees KR, Albers GW, et al (2000) Selfotel in acute ischemic stroke possible neurotoxic effects of an NMDA antagonist. Stroke 31 347-354 DeKeyser J (1991) Excitotoxic mechanisms may be involved in the pathophysiology of tardive dyskinesia. Clin Neuropharmacol 14 562-565 Del Dotto P, Pavese N, Gambaccini G, et al (2001) Intravenous amantadine improves levodopa-induced dyskinesias an acute double-blind placebo-controlled study. Mov Disord 16 515-520... [Pg.288]

Our emphasis on the interplay among excitotoxicity, oxidative stress, and neuroinflammation does not rule out the participation of other mechanisms involved in neural cell injury. However, it is timely and appropriate to apply the concept of interplay among excitotoxicity, oxidative stress, and neuroinflammation to neural cell injury in acute neural trauma and neurodegenerative diseases. Lack of coordination among the above parameters may control the time taken by neural cells to... [Pg.188]

Morimoto E., Murasugi T., and Oda T. (2002). Acute neuroinflammation exacerbates excitotoxicity in rat hippocampus in vivo. Exp. Neurol. 177 95-104. [Pg.236]


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