Relevant bibliographies by topics / Excitotoxicity

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Excitotoxicity'

Author: Grafiati
Published: 4 June 2021
Last updated: 25 July 2025

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Journal articles on the topic "Excitotoxicity"

1

Nicotera, Pierluigi, and Marcel Leist. "Excitotoxicity." Cell Death & Differentiation 4, no. 6 (1997): 517–18. http://dx.doi.org/10.1038/sj.cdd.4400274.

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Haglid, K. G., S. Wang, Y. Qiner, and A. Hamberger. "Excitotoxicity." Molecular Neurobiology 9, no. 1-3 (1994): 259–63. http://dx.doi.org/10.1007/bf02816125.

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Rothstein, J. D. "Excitotoxicity hypothesis." Neurology 47, Issue 4, Supplement 2 (1996): 19S—26S. http://dx.doi.org/10.1212/wnl.47.4_suppl_2.19s.

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Novelli, A., and R. A. Tasker. "Excitotoxicity - Introduction." Amino Acids 23, no. 1-3 (2002): 9–10. http://dx.doi.org/10.1007/s007260200028.

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Mohd Sairazi, Nur Shafika, K. N. S. Sirajudeen, Mohd Asnizam Asari, Mustapha Muzaimi, Swamy Mummedy, and Siti Amrah Sulaiman. "Kainic Acid-Induced Excitotoxicity Experimental Model: Protective Merits of Natural Products and Plant Extracts." Evidence-Based Complementary and Alternative Medicine 2015 (2015): 1–15. http://dx.doi.org/10.1155/2015/972623.

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Excitotoxicity is well recognized as a major pathological process of neuronal death in neurodegenerative diseases involving the central nervous system (CNS). In the animal models of neurodegeneration, excitotoxicity is commonly induced experimentally by chemical convulsants, particularly kainic acid (KA). KA-induced excitotoxicity in rodent models has been shown to result in seizures, behavioral changes, oxidative stress, glial activation, inflammatory mediator production, endoplasmic reticulum stress, mitochondrial dysfunction, and selective neurodegeneration in the brain upon KA administrati
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Stahl, Stephen M. "Excitotoxicity and Neuroprotection." Journal of Clinical Psychiatry 58, no. 6 (1997): 247–48. http://dx.doi.org/10.4088/jcp.v58n0601.

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Fernández-Sánchez, Maria Teresa, and Antonello Novelli. "Neurotrophins and Excitotoxicity." Science 270, no. 5244 (1995): 2019. http://dx.doi.org/10.1126/science.270.5244.2019-a.

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Nicholls, D. G., S. L. Budd, M. W. Ward, and R. F. Castilho. "Excitotoxicity and mitochondria." Biochemical Society Symposia 66 (September 1, 1999): 55–67. http://dx.doi.org/10.1042/bss0660055.

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Excitotoxicity is the process whereby a massive glutamate release in the central nervous system in response to ischaemia or related trauma leads to the delayed, predominantly necrotic death of neurons. Excitotoxicity is also implicated in a variety of slow neurodegenerative disorders. Mitochondria accumulate much of the post-ischaemic calcium entering the neurons via the chronically activated N-methyl-d-aspartate receptor. This calcium accumulation plays a key role in the subsequent death of the neuron. Cultured cerebellar granule cells demonstrate delayed calcium de-regulation (DCD) followed
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Leigh, P. N., and B. S. Meldrum. "Excitotoxicity in ALS." Neurology 47, Issue 6, Supplement 4 (1996): 221S—227S. http://dx.doi.org/10.1212/wnl.47.6_suppl_4.221s.

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Krieglstein, J. "Excitotoxicity and neuroprotection." European Journal of Pharmaceutical Sciences 5, no. 4 (1997): 181–87. http://dx.doi.org/10.1016/s0928-0987(97)00276-5.

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Dissertations / Theses on the topic "Excitotoxicity"

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Chen, Yongmei. "Excitotoxicity in neurodegenerative disorders." free to MU campus, to others for purchase, 1998. http://wwwlib.umi.com/cr/mo/fullcit?p9901225.

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Scott, Michael Murray. "Development of in vitro models of NMDA excitotoxicity and assessment of excitotoxicity modulation by neurosteroids." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ36079.pdf.

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Giardina, Sarah Filippa 1974. "Neuropharmacology of kainate receptor-mediated excitotoxicity." Monash University, Dept. of Pharmacology, 2001. http://arrow.monash.edu.au/hdl/1959.1/8980.

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Soundarapandian, Mangala Meenakshi. "Glutamate Excitotoxicity in Epilepsy and Ischemia." Doctoral diss., University of Central Florida, 2007. http://digital.library.ucf.edu/cdm/ref/collection/ETD/id/3169.

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'Excitotoxicity' represents the excitatory amino acid mediated degeneration of neurons. Glutamate is the major excitatory neurotransmitter in the brain. Glutamate excitotoxicity has been implicated in a number of neurodegenerative disorders like Stroke, Epilepsy, Alzheimer's disease and traumatic brain injury. This neurotoxicity is summed up by the 'glutamate hypothesis' which describes the cause of neuronal cell death as an excessive release of glutamate causing over excitation of the glutamate receptors and subsequent increase in influx of calcium leading to cell death. An effort to countera
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Gladbach, Philip Amadeus Wilhelm. "The role of tau in excitotoxicity." Thesis, The University of Sydney, 2013. http://hdl.handle.net/2123/9557.

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Stroke is a leading cause of death. The majority are ischemic strokes resulting from acute focal brain infarction with sudden and persisting neurological deficits. This primary brain damage is followed by more substantial secondary destruction of surrounding areas (=penumbra). A major pathomechanism underlying penumbra formation is excitotoxicity, which results from over-excitation of glutaminergic synapses involving N-methyl-D-aspartate receptor signaling. Excitotoxicity also contributes to neurodegeneration in Alzheimer’s disease (AD), where the microtubule-associated protein tau deposits in
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Zhu, Shanshan. "Factors in glutamate excitotoxicity, inflammation and epilepsy." Thesis, University of British Columbia, 2011. http://hdl.handle.net/2429/39844.

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Studying the mechanisms underlying glutamate excitotoxicity and inflammatory responses provides hints to the pathology of neurological diseases such as epilepsy. In this dissertation I investigated the expression and function of Krüppel-like factor 4 (KLF4) in glutamate excitotoxicity. I also studied the distribution and the role of progranulin (PGRN) in inflammatory stimulation, in epilepsy and in astrocytes subjected to glutamate excitotoxicity. First, I studied the role of KLF4 and found that NMDA induced KLF4 expression in cultured neurons and in brain slices. Overexpression of KLF4 upregu
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Bakshi, Deeksha. "The role of NMDA receptors in excitotoxicity." Thesis, University of British Columbia, 2013. http://hdl.handle.net/2429/43907.

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NMDA receptors are glutamate-gated cation channels named after their prototypical selective agonist NMDA. The channels occur as multiple subtypes, which are formed from interactions between different receptor subunits. NMDA receptor subunits are classified into three families: NR1, NR2A-D, and NR3A, B. NMDA receptors are implicated in HD pathology. During HD, a subset of medium-sized aspiny interneurons in the striatum that co-localize SST, NPY, and the enzyme NOS are selectively spared. In contrast, medium-sized spiny cells that constitute 80 % of all striatal neurons undergo selective
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Jones, Paul A. "Modulation of kainate-induced excitotoxicity in rats." Thesis, University of Glasgow, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244361.

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Serzysko, Malgorzata. "Endocannabinoids and excitotoxicity: lessons from hypoglossal motoneurons." Doctoral thesis, SISSA, 2015. http://hdl.handle.net/20.500.11767/3908.

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Brainstem hypoglossal motoneurons (HMs) exclusively innervate tongue muscles and are severely damaged in the neurodegenerative disease called amyotrophic lateral sclerosis (ALS). One mechanism leading to such cell death is proposed to be glutamate-mediated excitotoxic stress. HMs are particularly vulnerable to excitotoxicity due to their expression of calcium-permeable α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-type glutamate receptors and scarcity of intracellular Ca2+ binding proteins like parvalbumin and calbindin. Indeed, blocking glutamate uptake in medullary slices can l
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Tannenberg, Rudi. "Excitotoxicity in Alzheimer disease : a synaptic terminal study /." [St. Lucia, Qld.], 2005. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe18741.pdf.

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Books on the topic "Excitotoxicity"

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Ferrarese, Carlo, and M. Flint Beal, eds. Excitotoxicity in Neurological Diseases. Springer US, 2004. http://dx.doi.org/10.1007/978-1-4419-8959-8.

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Farooqui, Akhlaq A. Neurochemical aspects of excitotoxicity. Springer, 2008.

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1955-, Ferrarese Carlo, and Beal Flint, eds. Excitotoxicity in neurological diseases: New therapeutic challenge. Kluwer Academic, 2004.

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4

Drew, Shelley. Hearing loss induced by bacterial meningitis: Investigations into the possible involvement of, (i) bacterial ototoxins, (ii) nitric oxide, excitotoxicity, and reactive oxygen species. University of Birmingham, 1999.

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Ferrarese, Carlo. Excitotoxicity in Neurological Diseases. Springer, 2012.

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Neurochemical Aspects of Excitotoxicity. Springer New York, 2008. http://dx.doi.org/10.1007/978-0-387-73023-3.

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Neurochemical Aspects of Excitotoxicity. Springer, 2007.

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Horrocks, Lloyd A., Akhlaq A. Farooqui, and Wei-Yi Ong. Neurochemical Aspects of Excitotoxicity. Springer, 2010.

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(Editor), Carlo Ferrarese, and M. Flint Beal (Editor), eds. Excitotoxicity in Neurological Diseases: New Therapeutic Challenge. Springer, 2003.

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Metzger, Emerson D., and Keith G. Halsey. Excitotoxicity: Fundamental Concepts, Pathophysiology and Treatment Strategies. Nova Science Publishers, Incorporated, 2013.

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Book chapters on the topic "Excitotoxicity"

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Hayashi, Nariyuki, and Dalton W. Dietrich. "Excitotoxicity." In Brain Hypothermia Treatment. Springer Japan, 2004. http://dx.doi.org/10.1007/978-4-431-53953-7_13.

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Mattson, Mark P. "Excitotoxicity." In Neurodegeneration. John Wiley & Sons, Ltd, 2017. http://dx.doi.org/10.1002/9781118661895.ch4.

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Lipton, Stuart A. "Excitotoxicity." In Neuroprotection. Wiley-VCH Verlag GmbH & Co. KGaA, 2005. http://dx.doi.org/10.1002/3527603867.ch14.

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Alagha, Julie, Sulaiman Alshaar, and Zane Deliu. "Excitotoxicity." In Apoptosis and Beyond. John Wiley & Sons, Inc., 2018. http://dx.doi.org/10.1002/9781119432463.ch10.

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Ellenbroek, Bart, Alfonso Abizaid, Shimon Amir, et al. "Excitotoxicity." In Encyclopedia of Psychopharmacology. Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_1263.

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Kim, A. H., G. A. Kerchner, and D. W. Choi. "Blocking Excitotoxicity." In CNS Neuroprotection. Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-662-06274-6_1.

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Evers, Martin, and Eric Hollander. "Excitotoxicity in Autism." In Autism. Humana Press, 2008. http://dx.doi.org/10.1007/978-1-60327-489-0_6.

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Choi, D. W. "Excitotoxicity and Stroke." In Brain Ischemia. Springer London, 1995. http://dx.doi.org/10.1007/978-1-4471-2073-5_4.

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Kerchner, G. A., A. H. Kim, and D. W. Choi. "Glutamate-Mediated Excitotoxicity." In Ionotropic Glutamate Receptors in the CNS. Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-662-08022-1_14.

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Rahman, Abdur, and Gilles J. Guillemin. "Lead and Excitotoxicity." In Handbook of Neurotoxicity. Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-15080-7_142.

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Conference papers on the topic "Excitotoxicity"

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Lee, Yu-Hsuan, Yi-Ke Lin, Ta-Ching Chen, and Lih-Chu Chiou. "Novel glaucoma therapy rescuing excitotoxicity in an ischemia-reperfusion mice model." In Mechanisms of Photobiomodulation Therapy XIX, edited by James D. Carroll, Ann Liebert, and Jeri-Anne Lyons. SPIE, 2025. https://doi.org/10.1117/12.3054809.

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Lin, Xiaotong, and Tingting Yan. "ALZHEIMER'S DISEASE: MECHANISMS OF TAU AND AMYLOID BETA-INDUCED EXCITOTOXICITY." In 2016 International Conference on Biotechnology and Medical Science. WORLD SCIENTIFIC, 2016. http://dx.doi.org/10.1142/9789813145870_0055.

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Henningsen, Jo B., Barbara Baldo, Maria Björkqvist, and Åsa Petersén. "A54 The role of excitotoxicity for neuropathology in the lateral hypothalamus in mouse models of huntington disease." In EHDN 2018 Plenary Meeting, Vienna, Austria, Programme and Abstracts. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/jnnp-2018-ehdn.52.

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Konorova, Irina, and Kristina Glebova. "INFLUENCE OF OXIDATIVE MODIFICATION OF EXTRACELLULAR DNA ON THE SURVIVAL OF CEREbellar GRANULAR NEURONS IN GLUTAMATE EXCITOTOXICITY." In XX INTERNATIONAL INTERDISCIPLINARY CONGRESS NEUROSCIENCE FOR MEDICINE AND PSYCHOLOGY. LCC MAKS Press, 2024. http://dx.doi.org/10.29003/m3926.sudak.ns2024-20/153.

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Mehta, Tanmay, Annie McDermott, Nicolas Daviaud, and Saud Sadiq. "Long-term Culture of Cerebral Organoid Reveals Disruption of Glial Cell Differentiation and Glutamate Excitotoxicity in Multiple Sclerosis. (P2-3.002)." In 2023 Annual Meeting Abstracts. Lippincott Williams & Wilkins, 2023. http://dx.doi.org/10.1212/wnl.0000000000202430.

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Pershina, Ekaterina, Irina Chernomorets, Natalia Zhyikova, and Anna Gardzhuk. "EFFECT OF COMBINED PHARMACOLOGICAL SUPPRESSION OF EXCITOTOXICITY BY MEMANTINE AND POSITIVE MODULATION OF GROUP III METABOTROPIC GLUTAMATE RECEPTORS ON TRIMETHYLTIN CHLORIDE-INDUCED NEURODEGENERATION IN THE RAT BRAIN." In XVIII INTERNATIONAL INTERDISCIPLINARY CONGRESS NEUROSCIENCE FOR MEDICINE AND PSYCHOLOGY. LCC MAKS Press, 2022. http://dx.doi.org/10.29003/m2886.sudak.ns2022-18/268-269.

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Leão, Arthur Ventura Martins, Alexandre Leite Rodrigues de Oliveira, and Luciana Politti Cartarozzi. "Neuroprotection by memantine after compressive spinal root lesion." In XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.383.

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Introduction: Compressive root lesions are characterized by changes in the spinal cord microenvironment, which include motoneuron chromatolysis and degeneration, chronic gliosis, and glutamatergic excitotoxicity. Since excessive NMDAr stimulation by glutamate leads to neuronal degeneration, the use of NMDAr antagonists has been proposed as a promissing treatment central and peripheral nerve injuries. Objective: The present study aimed to investigate the neuroprotective effects of memantine, following compressive spinal root axotomy. Methods: Adult C57BL/6J mice were subjected to unilateral ven
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Reports on the topic "Excitotoxicity"

1

Smith, Yoland. Kainate Receptors in the Striatum: Implications for Excitotoxicity in Huntington's Disease. Defense Technical Information Center, 2004. http://dx.doi.org/10.21236/ada426787.

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Smith, Yoland. Kainate Receptors in the Striatum: Implications for Excitotoxicity in Huntington's Disease. Defense Technical Information Center, 2003. http://dx.doi.org/10.21236/ada421025.

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