The DOI matches its Crossref record; 197 of the 197 references it cites were found in a registry or an index.
Molecular Mechanisms of Glutamate Receptor-Mediated Excitotoxic Neuronal Cell Death
Abstract
Excitotoxicity is one of the most extensively studied processes of neuronal cell death, and plays an important role in many central nervous system (CNS) diseases, including CNS ischemia, trauma, and neurodegenerative disorders. First described by Olney, excitotoxicity was later characterized as an excessive synaptic release of glutamate, which in turn activates postsynaptic glutamate receptors. While almost every glutamate receptor subtype has been implicated in mediating excitotoxic cell death, it is generally accepted that the N-methyl-D-aspartate (NMDA) subtypes play a major role, mainly owing to their high calcium (Ca2+) permeability. However, other glutamate receptor subtypes such as 2-amino-3-(3-hydroxy-5-methylisoxazol-4-yl) propionate (AMPA) or kainate receptors have also been attributed a critical role in mediating excitotoxic neuronal cell death. Although the molecular basis of glutamate toxicity is uncertain, there is general agreement that it is in large part Ca(2+)-dependent. The present review is aimed at summarizing the molecular mechanisms of NMDA receptor and AMPA/kainate receptor-mediated excitotoxic neuronal cell death.
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“Excitotoxicity is considered to be a major mechanism of neuronal death that occurs due to intracellular calcium overload followed by the activation of various cell death pathways41.”
From Microglia protect against brain injury and their selective elimination dysregulates neuronal network activity after stroke (2016) · cites this paper as [41]
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Cites
Glutamate neurotoxicity and diseases of the nervous system
Choi, D. W. (1988) · Neuron · doi:10.1016/0896-6273(88)90162-6 · Cited by 8,184
Hollmann, M., & Heinemann, S. F. (1994) · Annual Review of Neuroscience · doi:10.1146/annurev.ne.17.030194.000335 · Cited by 4,056
Monyer, H., Burnashev, N., Laurie, D. J., Sakmann, B., & Seeburg, P. H. (1994) · Neuron · doi:10.1016/0896-6273(94)90210-0 · Cited by 3,535
Heteromeric NMDA receptors: molecular and functional distinction of subtypes
Monyer, H., Sprengel, R., Schoepfer, R., Herb, A., Higuchi, M., Lomeli, H., Burnashev, N., Sakmann, B., & Seeburg, P. H. (1992) · Science · doi:10.1126/science.256.5060.1217 · Cited by 2,541
Structure and Regulation of Voltage-Gated Ca 2+ Channels
Catterall, W. A. (2000) · Annual Review of Cell and Developmental Biology · doi:10.1146/annurev.cellbio.16.1.521 · Cited by 2,344
Domain Interaction Between NMDA Receptor Subunits and the Postsynaptic Density Protein PSD-95
Kornau, H., Schenker, L. T., Kennedy, M. B., & Seeburg, P. H. (1995) · Science · doi:10.1126/science.7569905 · Cited by 1,916
Brain Lesions, Obesity, and Other Disturbances in Mice Treated with Monosodium Glutamate
Olney, J. (1969) · Science · doi:10.1126/science.164.3880.719 · Cited by 1,885
Ionic dependence of glutamate neurotoxicity
Choi, D. W. (1987) · Journal of Neuroscience · doi:10.1523/jneurosci.07-02-00369.1987 · Cited by 1,854
Nitric oxide mediates glutamate-linked enhancement of cGMP levels in the cerebellum.
Bredt, D. S., & Snyder, S. H. (1989) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.86.22.9030 · Cited by 1,849
Ben-Ari, Y. (1985) · Neuroscience · doi:10.1016/0306-4522(85)90299-4 · Cited by 1,753
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Calcium, ATP, and ROS: a mitochondrial love-hate triangle
Brookes, P. S., Yoon, Y., Robotham, J. L., Anders, M. W., & Sheu, S.-S. (2004) · American Journal of Physiology-Cell Physiology · doi:10.1152/ajpcell.00139.2004 · Cited by 2,575
Regulated necrosis: the expanding network of non-apoptotic cell death pathways
Berghe, T. V., Linkermann, A., Jouan-Lanhouet, S., Walczak, H., & Vandenabeele, P. (2014) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm3737 · Cited by 1,735
Neuroinflammation: friend and foe for ischemic stroke
Jayaraj, R. L., Azimullah, S., Beiram, R., Jalal, F. Y., & Rosenberg, G. A. (2019) · Journal of Neuroinflammation · doi:10.1186/s12974-019-1516-2 · Cited by 1,479
CB1 Cannabinoid Receptors and On-Demand Defense Against Excitotoxicity
Marsicano, G., Goodenough, S., Monory, K., Hermann, H., Eder, M., Cannich, A., Azad, S. C., Cascio, M. G., Gutiérrez, S. O., van der Stelt, M., et al. (2003) · Science · doi:10.1126/science.1088208 · Cited by 1,208
Retinal ischemia: mechanisms of damage and potential therapeutic strategies
Osborne, N. N., Casson, R. J., Wood, J. P. M., Chidlow, G., Graham, M., & Melena, J. (2004) · Progress in Retinal and Eye Research · doi:10.1016/j.preteyeres.2003.12.001 · Cited by 1,072
Metadata
- Authors
- Sattler, R., & Tymianski, M.
- Affiliations
- Howard Hughes Medical Institute (US)
- Toronto Western Hospital (CA)
- Corresponding author
- Sattler, Rita
- Venue
- Molecular Neurobiology
- Published
- 2001
- Volume
- 24
- Issue
- 1-3
- Pages
- 107-130
- ISSN
- 0893-7648 (ISSN-L)
- OpenAlex
- W2027397876
- Cited by
- 537
- References
- 197
- Citations by year
- 2026: 5 · 2025: 10 · 2024: 11 · 2023: 15 · 2022: 14 · 2021: 15 · 2020: 22 · 2019: 18 · 2018: 23 · 2017: 22 · 2016: 25 · 2015: 27 · 2014: 23 · 2013: 22 · 2012: 24
- FWCI
- 8.52
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Molecular Neurobiology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01ns039060-03)
- National Institute of Neurological Disorders and Stroke (R01 NS 39060)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Amino Acid Enzymes and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- excitotoxicity, neuronal cell death, glutamate receptors, NMDA receptor, AMPA receptors, kainate receptors, calcium signaling, neurodegenerative diseases
- MeSH terms
- Animals, Central Nervous System Diseases, Humans, Neurons, Neurotoxins, Cell Death, Receptors, Glutamate
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