Relevant bibliographies by topics / Excitotoxicity

Academic literature on the topic 'Excitotoxicity'

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Published: 4 June 2021
Last updated: 25 May 2024

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Journal articles on the topic "Excitotoxicity"

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Nicotera, Pierluigi, and Marcel Leist. "Excitotoxicity." Cell Death & Differentiation 4, no. 6 (August 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 (August 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 (October 1, 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 (September 1, 2002): 9–10. http://dx.doi.org/10.1007/s007260200028.

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Stahl, Stephen M. "Excitotoxicity and Neuroprotection." Journal of Clinical Psychiatry 58, no. 6 (June 15, 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 (December 22, 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 by necrosis upon exposure to glutamate. DCD is unaffected by the ATP synthase inhibitor oligomycin but is inhibited by the further addition of a respiratory chain inhibitor to depolarize the mitochondria and inhibit mitochondrial calcium accumulation without depleting ATP [Budd and Nicholls (1996) J. Neurochem. 67, 2282-2291]. Mitochondrial depolarization paradoxically decreases the cytoplasmic calcium elevation following glutamate addition, probably due to an enhanced calcium efflux from the cell. Cells undergo immediate calcium de-regulation in the presence of glutamate if the respiratory chain is inhibited; this is due to ATP depletion following ATP synthase reversal and can be reversed by oligomycin. In contrast, DCD is irreversible. Elevated cytoplasmic calcium is not excitotoxic as long as mitochondria are depolarized; alternative substrates do not rescue cells about to undergo DCD, suggesting that glycolytic failure is not involved. Mitochondria in situ remain sufficiently polarized during granule cell glutamate exposure to continue to generate ATP and show a classic mitochondrial state 3-state 4 hyperpolarization on inhibiting ATP synthesis; mitochondrial depolarization follows, and may be a consequence of rather than a cause of DCD. In addition, our studies show no evidence of the mitochondrial permeability transition prior to DCD. The mitochondrial generation of superoxide anions is enhanced during glutamate exposure and a working hypothesis is that DCD may be caused by oxidative damage to calcium extrusion pathways at the plasma membrane.
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Leigh, P. N., and B. S. Meldrum. "Excitotoxicity in ALS." Neurology 47, Issue 6, Supplement 4 (December 1, 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 (July 1997): 181–87. http://dx.doi.org/10.1016/s0928-0987(97)00276-5.

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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 administration. Recently, there is an emerging trend to search for natural sources to combat against excitotoxicity-associated neurodegenerative diseases. Natural products and plant extracts had attracted a considerable amount of attention because of their reported beneficial effects on the CNS, particularly their neuroprotective effect against excitotoxicity. They provide significant reduction and/or protection against the development and progression of acute and chronic neurodegeneration. This indicates that natural products and plants extracts may be useful in protecting against excitotoxicity-associated neurodegeneration. Thus, targeting of multiple pathways simultaneously may be the strategy to maximize the neuroprotection effect. This review summarizes the mechanisms involved in KA-induced excitotoxicity and attempts to collate the various researches related to the protective effect of natural products and plant extracts in the KA model of neurodegeneration.
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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 counteract this neurotoxicity has lead to the development of glutamate receptor antagonists that can effectively serve as neuroprotective agents. Nevertheless, the downside to these drugs has been the side effects observed in clinical trial patients due to their disruptive action on the physiological function of these receptors like learning and memory. This work was undertaken to identify targets that can effectively be used to treat excitotoxicity without affecting any normal physiological functions. In one approach, (chapter I) we have identified the KATP channels as an effective modulator of epileptogenesis. In another approach, (Chapter II) we show that targeting the AMPA receptor subunit GluR2 is a practical strategy for stroke therapy. KATP channels that are gated by intracellular ATP/ADP concentrations are a unique subtype of potassium channels and play an essential role in coupling intracellular metabolic events to electrical activity. Opening of KATP channels during energy deficits in the central nervous system (CNS) induces efflux of potassium ions and in turn hyperpolarizes neurons. Thus, activation of KATP channels is thought to be able to counteract excitatory insults and protect against neuronal death. Here, we show that, functional Kir6.1 channels are located at excitatory pre-synaptic terminals as a complex with type-1 Sulfonylurea receptors (SUR1) in the hippocampus. The mutant mice with deficiencies in expressing the Kir6.1 or the SUR1 gene are more vulnerable to generation of epileptic form of seizures, compared to wild-type controls. Whole-cell patch clamp recordings demonstrate that genetic deletion of the Kir6.1/SUR1 channels enhances glutamate release at CA3 synapses. Hence, expression of functional Kir6.1/SUR1 channels inhibits seizure responses and possibly acts via limiting excitatory glutamate release. In addition to epilepsy, ischemic stroke is a leading cause of death in developed countries. A critical feature of this disease is a highly selective pattern of neuronal loss; certain identifiable subsets of neurons, particularly CA1 pyramidal neurons in the hippocampus are severely damaged, whereas others remain intact. A key step in this selective neuronal injury is Ca2+/Zn2+ entry into vulnerable neurons through [alpha]-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptor channels, a principle subtype of glutamate receptors. AMPA receptor channels are assembled from glutamate receptor (GluR) -1, -2, -3, and -4 subunits. Circumstance data have indicated that the GluR2 subunits dictate Ca2+/Zn2+ permeability of AMPA receptor channels and gate injurious Ca2+/Zn2+ signals in vulnerable neurons. Here we show that ischemic insults induce toxic Ca2+ entry through AMPA receptors into vulnerable neurons by modification of GluR2 RNA editing. Thus, targeting of GluR2 subunit can be considered as a promising target for stroke therapy.
Ph.D.
Department of Biomolecular Science
Burnett College of Biomedical Sciences
Biomolecular Sciences PhD
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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 neurons. Here, I show that reducing tau levels can prevent deficits in different AD mouse models. Furthermore, I show that tau-deficient mice (tau-/-) are protected from excitotoxic brain damage following induced seizure and stroke by middle cerebral artery occlusion and from progression of neurological deficits. Gene profiling indicated differential mitogen-activated protein kinase (MAPK) signaling induced by excitotoxic stress in tau-/- mice, with absent Ras and subsequent extracellular signal-regulated kinase (ERK) activation and immediate early gene induction. Accordingly, inhibition of MAP/ERK kinase 1/2 reduced MCAO-induced infarct size and neurological deficits in wild-type mice to the same degree as tau-depletion. Hence, my findings suggest tau dependent Ras/ERK activation drives excitotoxic secondary brain damage in stroke, implicating tau as a possible therapeutic target in acute brain damage beyond AD.
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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 upregulated cyclin D1 and downregulated p21Waf1/Cip1, suggesting the neuron’s progression into cell cycle. KLF4 expression also induced the cleavage of caspase-3 under conditions of a subtoxic dose of NMDA. Thus our work suggests that KLF4 might play a role in NMDA-induced apoptosis. Second, I studied the function of PGRN and observed that PGRN was enhanced in activated microglia after pilocarpine-induced epilepsy. In mixed cultures, lipopolysaccharide (LPS) also induced PGRN expression. Recombinant PGRN protein promoted microglial activation in the dentate gyrus after epilepsy and in purified microglial cell culture. PGRN was also required for LPS-induced microglial migration. Our work suggests that PGRN may contribute to microglial activation after epileptic and inflammatory insults. Third, I performed a preliminary study on the role of PGRN in purified culture of astrocytes. I found that our cultured astrocytes express PGRN, and PGRN was required for glutamate-induced lactate release. PGRN was also involved in glutamate-induced glucose uptake and participated in the regulation of monocarboxylate transporter 1 (MCT1) expression in excitotoxic conditions. Our findings suggest that PGRN may be involved in glutamate-evoked increase of glycolysis in cultured astrocytes. In conclusion, our findings provide insights into factors involved in glutamate excitotoxicity, inflammation, and epilepsy.
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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 neurodegeneration. While it was suggested that the interneurons survive because they lack NMDA receptors, studies including from our lab have shown the presence of NR1 in SST-positive striatal neurons. The finding of NR1 expression and co-localization with SST-positive neurons indicates that NMDA receptor-induced toxicity may be regulated in a receptor-specific manner. Therefore, the present study was conducted to investigate whether NMDA application leads to toxicity that is receptor-specific in HEK293 cells stably transfected with NR1, NR2A, or NR2B. The main findings of this study indicate that NMDA application causes cell death, which varies in intensity and nature, depending upon the NMDA concentration applied, and the receptor-type expressed by the cells. Cells expressing NR1 were found to undergo apoptosis but not necrosis, while cells expressing NR2A/NR2B underwent both apoptosis and necrosis in a receptor-specific manner. In cells expressing NR2A/NR2B, exposure to low concentrations of NMDA resulted in cell death that was predominantly apoptotic. In contrast, exposure to high concentrations of NMDA produced mostly necrosis. In cells expressing NR1, NMDA application caused apoptosis, which exhibited a gradual increase in response to greater concentrations of NMDA. In addition, cell death through apoptosis and/or necrosis was determined to be the greatest at all NMDA concentrations in cells expressing NR2B, followed by those expressing NR2A, and then NR1. Taken together, these results indicate that the activation of receptors formed by NR1, NR2A, or NR2B have different toxic consequences. Thus, the selective neurodegeneration observed during HD may be due to the variation in expression levels of NR1, NR2A, and NR2B between medium-sized aspiny interneurons and medium-sized spiny projection neurons.
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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 lead to pathological bursting and motoneuron damage. The endocannabinoid system is widely distributed in the brain and is believed to be an important regulator of synaptic transmission. Several studies reported neuroprotection mediated by the endocannabinoid system in such pathological insults like brain ischemia, traumatic brain injury or excitotoxicity. Moreover, in ALS animal models, up-regulation of the endocannabinoid system has been detected, suggesting it can play a role during disease development. Thus, detailed information on how the endocannabinoid system can affect cells during pathological insults like excitotoxicity is a valuable asset for future investigations of novel therapy approaches for ALS. The objective of this work was to investigate the effect of modulation of the endocannabinoid system during excitotoxic stress in hypoglossal motoneurons in vitro. Thin medullary slices (for electrophysiology and viability assay) or whole brainstem isolates (for Western Blot) from postnatal Wistar rats were used. Each slice/brainstem containing hypoglossal nuclei was transferred to a recording/incubation chamber and superfused with oxygenated Krebs solution. Excitotoxic stress was evoked by application of DL-TBOA (DL-threo-β-benzyloxyaspartic acid, 50 μM), a potent and selective inhibitor of excitatory amino acid transporters, with consequent build-up of extracellular glutamate. It was observed that modulation of endocannabinoid CB1 receptor (CB1R) function affected TBOA-evoked bursting, an event previously correlated with TBOA toxicity. Co-application of the endocannabinoid anandamide (AEA, 10 μM), a CB1R agonist, with TBOA resulted in lowered probability of the occurrence of pathological bursting, whereas co-application of the CB1R antagonist AM251 (10 μM) disrupted TBOA-induced bursts, leading to their “fragmentation”. Furthermore, AEA significantly decreased the frequency of spontaneous excitatory postsynaptic currents (sEPSCs) isolated by co-application of bicuculline and strychnine (10 μM and 0.4 μM, respectively) and caused occurrence of biphasic activity in spontaneous inhibitory postsynaptic currents (sIPSCs; isolated by co-application of DNQX and APV at 10 μM and 50 μM, respectively) in some of the recorded cells. AM251 caused a decrease in the frequency of sIPSCs, but during application of bicuculline and strychnine it evoked activity which partly resembled bursting observed during TBOA application. Moreover, co-application of AEA with TBOA significantly decreased the number of damaged propidium iodide-positive cells with respect to counterstained Hoechst 33342-positive cells, which suggests a protective effect of this CB1R agonist against TBOA-induced toxicity. In addition, Western blot analysis showed a significant increase in CB1R protein levels after only 4 hours of TBOA incubation, indicating that the endocannabinoid system is activated during this excitotoxic insult. We suggest that a likely role of the endocannabinoid system in our brainstem preparation is to counteract the effects and consequences of elevated glutamate levels in the extracellular compartment.
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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. Boston, MA: 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. New York: Springer, 2008.

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

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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. Birmingham: University of Birmingham, 1999.

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

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

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

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Neurochemical Aspects of Excitotoxicity. Springer, 2007.

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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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Excitotoxicity in neurological diseases: New therapeutic challenge. Boston, MA: Kluwer Academic Publishers, 2003.

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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, 23. Tokyo: 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, 37–45. Oxford, UK: John Wiley & Sons, Ltd, 2017. http://dx.doi.org/10.1002/9781118661895.ch4.

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Lipton, Stuart A. "Excitotoxicity." In Neuroprotection, 291–313. Weinheim, FRG: 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, 197–204. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2018. http://dx.doi.org/10.1002/9781119432463.ch10.

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Ellenbroek, Bart, Alfonso Abizaid, Shimon Amir, Martina de Zwaan, Sarah Parylak, Pietro Cottone, Eric P. Zorrilla, et al. "Excitotoxicity." In Encyclopedia of Psychopharmacology, 516. Berlin, Heidelberg: 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, 3–36. Berlin, Heidelberg: 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, 133–45. Totowa, NJ: 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, 29–36. London: 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, 443–69. Berlin, Heidelberg: 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, 1–39. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-71519-9_142-1.

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Conference papers on the topic "Excitotoxicity"

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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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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 ventral root crush (VRC) and divided into four groups: VRC+Vehicle, VRC+Memantine 30 mg/kg, 45 mg/kg, and 60 mg/kg. The treatment was administered orally for 14 days, starting immediately after injury. Twenty-eight days after the lesion, lumbar intumescences were collected and processed for motoneuron counting (toluidine blue staining), together with astrogliosis and microglial reaction assessment (immunohistochemistry for GFAP and Iba-1, respectively). The protocols for animal use and handling were approved by the local ethical committee (CEUA/UNICAMP, protocol no 5740-1). Results: Memantine rescued spinal motoneurons at all the studied doses when compared with the vehicle counterpart, being the 45 mg/kg group the most effective (P < 0.001). Memantine also downregulated microglial reactions at the doses of 45 mg/kg and 60 mg/kg (P < 0.01, and P < 0.05, respectively). Astrogliosis also decreased in all treated groups as compared to the control (P < 0.01). Conclusions: The memantine has a significant antiinflammatory effect on glial cells, coupled with neuroprotection of motoneurons, indicating a possible translation to the clinic.
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Reports on the topic "Excitotoxicity"

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

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