Literature DB >> 1361523

Excitotoxic cell death.

D W Choi1.   

Abstract

Excitotoxicity 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. Excitotoxicity has substantial cellular specificity and, in most cases, is mediated by glutamate receptors. On average, NMDA receptors activation may be able to trigger lethal injury more rapidly than AMPA or kainate receptor activation, perhaps reflecting a greater ability to induce calcium influx and subsequent cellular calcium overload. It is possible that excitotoxic death may share some mechanisms with other forms of neuronal death.

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Year:  1992        PMID: 1361523     DOI: 10.1002/neu.480230915

Source DB:  PubMed          Journal:  J Neurobiol        ISSN: 0022-3034


  480 in total

1.  Synaptically driven calcium transients via nicotinic receptors on somatic spines.

Authors:  R D Shoop; K T Chang; M H Ellisman; D K Berg
Journal:  J Neurosci       Date:  2001-02-01       Impact factor: 6.167

2.  Vitamin D hormone confers neuroprotection in parallel with downregulation of L-type calcium channel expression in hippocampal neurons.

Authors:  L D Brewer; V Thibault; K C Chen; M C Langub; P W Landfield; N M Porter
Journal:  J Neurosci       Date:  2001-01-01       Impact factor: 6.167

3.  Glutamate receptor requirement for neuronal death from anoxia-reoxygenation: an in Vitro model for assessment of the neuroprotective effects of estrogens.

Authors:  L L Zaulyanov; P S Green; J W Simpkins
Journal:  Cell Mol Neurobiol       Date:  1999-12       Impact factor: 5.046

4.  Rescue of cerebellar granule cells from death in weaver NR1 double mutants.

Authors:  P Jensen; D J Surmeier; D Goldowitz
Journal:  J Neurosci       Date:  1999-09-15       Impact factor: 6.167

5.  Regulation of Na+,K+-ATPase by persistent sodium accumulation in adult rat thalamic neurones.

Authors:  V V Senatorov; P K Stys; B Hu
Journal:  J Physiol       Date:  2000-06-01       Impact factor: 5.182

6.  Caspase-mediated degradation of AMPA receptor subunits: a mechanism for preventing excitotoxic necrosis and ensuring apoptosis.

Authors:  G W Glazner; S L Chan; C Lu; M P Mattson
Journal:  J Neurosci       Date:  2000-05-15       Impact factor: 6.167

7.  Cytoskeletal links of neuronal acetylcholine receptors containing alpha 7 subunits.

Authors:  R D Shoop; N Yamada; D K Berg
Journal:  J Neurosci       Date:  2000-06-01       Impact factor: 6.167

8.  The mitogen-activated protein kinase pathway mediates estrogen neuroprotection after glutamate toxicity in primary cortical neurons.

Authors:  C A Singer; X A Figueroa-Masot; R H Batchelor; D M Dorsa
Journal:  J Neurosci       Date:  1999-04-01       Impact factor: 6.167

9.  Oxidative glutamate toxicity can be a component of the excitotoxicity cascade.

Authors:  D Schubert; D Piasecki
Journal:  J Neurosci       Date:  2001-10-01       Impact factor: 6.167

10.  Subtypes of NMDA receptors in new-born rat hippocampal granule cells.

Authors:  Juan C Piña-Crespo; Alasdair J Gibb
Journal:  J Physiol       Date:  2002-05-15       Impact factor: 5.182

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