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Artykuły w czasopismach na temat „Excitotoxicity”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 25 lipca 2025

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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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2

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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3

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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4

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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6

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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8

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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9

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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10

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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11

Zheng, Xiang-Yu, Hong-Liang Zhang, Qi Luo, and Jie Zhu. "Kainic Acid-Induced Neurodegenerative Model: Potentials and Limitations." Journal of Biomedicine and Biotechnology 2011 (2011): 1–10. http://dx.doi.org/10.1155/2011/457079.

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Excitotoxicity is considered to be an important mechanism involved in various neurodegenerative diseases in the central nervous system (CNS) such as Alzheimer's disease (AD). However, the mechanism by which excitotoxicity is implicated in neurodegenerative disorders remains unclear. Kainic acid (KA) is an epileptogenic and neuroexcitotoxic agent by acting on specific kainate receptors (KARs) in the CNS. KA has been extensively used as a specific agonist for ionotrophic glutamate receptors (iGluRs), for example, KARs, to mimic glutamate excitotoxicity in neurodegenerative models as well as to d

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12

Liao, Rick, Thomas R. Wood, and Elizabeth Nance. "Nanotherapeutic modulation of excitotoxicity and oxidative stress in acute brain injury." Nanobiomedicine 7 (January 1, 2020): 184954352097081. http://dx.doi.org/10.1177/1849543520970819.

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Excitotoxicity is a primary pathological process that occurs during stroke, traumatic brain injury (TBI), and global brain ischemia such as perinatal asphyxia. Excitotoxicity is triggered by an overabundance of excitatory neurotransmitters within the synapse, causing a detrimental cascade of excessive sodium and calcium influx, generation of reactive oxygen species, mitochondrial damage, and ultimately cell death. There are multiple potential points of intervention to combat excitotoxicity and downstream oxidative stress, yet there are currently no therapeutics clinically approved for this spe

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13

Ertugrul, Muhammed, Ufuk Okkay, Yesim Yeni, et al. "Nicorandil mitigates glutamate excitotoxicity in primary cultured neurons." Medicine Science | International Medical Journal 13, no. 1 (2024): 43. http://dx.doi.org/10.5455/medscience.2023.07.112.

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Excitotoxicity, caused by the excessive release of glutamate, leads to the activation of the apoptotic process, making it a crucial factor in age-related neurodegenerative diseases. The aim of this study was to investigate the potential of nicorandil to prevent glutamate excitotoxicity and reduce oxidative stress in the brain by analyzing the effects of nicorandil on primary cortex neurons. The study used primary neuron cultures from newborn Sprague-Dawley rats to examine the impact of nicorandil on cell viability, Superoxide Dismutase, Catalase, Glutathione activity, Malondialdehyde levels, t

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14

Yalçın, G. Dönmez, and M. Colak. "SIRT4 prevents excitotoxicity via modulating glutamate metabolism in glioma cells." Human & Experimental Toxicology 39, no. 7 (2020): 938–47. http://dx.doi.org/10.1177/0960327120907142.

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Excitotoxicity is the presence of excessive glutamate, which is normally taken up by glutamate transporters on astrocytes. Glutamate transporter 1 (GLT-1) is the major transporter on glia cells clearing more than 90% of the glutamate. Sirtuin 4 (SIRT4) is a mitochondrial sirtuin which is expressed in the brain. Previously, it was shown that loss of SIRT4 leads to a more severe reaction to kainic acid, an excitotoxic agent, and also decreased GLT-1 expression in the brain. In this study, we aimed to investigate whether overexpression of SIRT4 is protective against excitotoxicity in glia cells.

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15

Zhuang, Dongli, Rong Zhang, Haiyang Liu, and Yi Dai. "A Small Natural Molecule S3 Protects Retinal Ganglion Cells and Promotes Parkin-Mediated Mitophagy against Excitotoxicity." Molecules 27, no. 15 (2022): 4957. http://dx.doi.org/10.3390/molecules27154957.

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Glutamate excitotoxicity may contribute to retinal ganglion cell (RGC) degeneration in glaucoma and other optic neuropathies, leading to irreversible blindness. Growing evidence has linked impaired mitochondrial quality control with RGCs degeneration, while parkin, an E3 ubiquitin ligase, has proved to be protective and promotes mitophagy in RGCs against excitotoxicity. The purpose of this study was to explore whether a small molecule S3 could modulate parkin-mediated mitophagy and has therapeutic potential for RGCs. The results showed that as an inhibitor of deubiquitinase USP30, S3 protected

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16

Hanley, Daniel F. "Multiple mechanisms of excitotoxicity." Critical Care Medicine 27, no. 3 (1999): 451–52. http://dx.doi.org/10.1097/00003246-199903000-00003.

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17

Stern, Peter. "Interface targeting skirts excitotoxicity." Science 370, no. 6513 (2020): 182.16–184. http://dx.doi.org/10.1126/science.370.6513.182-p.

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18

Raymond, Lynn A. "Excitotoxicity in Huntington disease." Clinical Neuroscience Research 3, no. 3 (2003): 121–28. http://dx.doi.org/10.1016/s1566-2772(03)00054-9.

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19

Mayer, Mark L., and Gary L. Westbrook. "Cellular mechanisms underlying excitotoxicity." Trends in Neurosciences 10, no. 2 (1987): 59–61. http://dx.doi.org/10.1016/0166-2236(87)90023-3.

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20

Matute, Carlos, Elena Alberdi, Gaskon Ibarretxe, and Marı́a Victoria Sánchez-Gómez. "Excitotoxicity in glial cells." European Journal of Pharmacology 447, no. 2-3 (2002): 239–46. http://dx.doi.org/10.1016/s0014-2999(02)01847-2.

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21

Ikonomidou, Chrysanthy, and Lechoslaw Turski. "Excitotoxicity and neurodegenerative diseases." Current Opinion in Neurology 8, no. 6 (1995): 487. http://dx.doi.org/10.1097/00019052-199512000-00017.

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22

Whetsell, William O. "Current Concepts of Excitotoxicity." Journal of Neuropathology and Experimental Neurology 55, no. 1 (1996): 1–13. http://dx.doi.org/10.1097/00005072-199601000-00001.

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23

GREENE, J., and J. GREENAMYRE. "Bioenergetics and glutamate excitotoxicity." Progress in Neurobiology 48, no. 6 (1996): 613–34. http://dx.doi.org/10.1016/0301-0082(96)00006-8.

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24

Szydlowska, Kinga, and Michael Tymianski. "Calcium, ischemia and excitotoxicity." Cell Calcium 47, no. 2 (2010): 122–29. http://dx.doi.org/10.1016/j.ceca.2010.01.003.

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25

Leist, Marcel, and Pierluigi Nicotera. "Apoptosis, Excitotoxicity, and Neuropathology." Experimental Cell Research 239, no. 2 (1998): 183–201. http://dx.doi.org/10.1006/excr.1997.4026.

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26

Johnston, Michael V. "Excitotoxicity in neonatal hypoxia." Mental Retardation and Developmental Disabilities Research Reviews 7, no. 4 (2001): 229–34. http://dx.doi.org/10.1002/mrdd.1032.

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27

Yoshioka, Akira, Brian Bacskai, and David Pleasure. "Pathophysiology of oligodendroglial excitotoxicity." Journal of Neuroscience Research 46, no. 4 (1996): 427–37. http://dx.doi.org/10.1002/(sici)1097-4547(19961115)46:4<427::aid-jnr4>3.0.co;2-i.

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28

Aarts, Michelle M., Mark Arundine, and Michael Tymianski. "Novel concepts in excitotoxic neurodegeneration after stroke." Expert Reviews in Molecular Medicine 5, no. 30 (2003): 1–22. http://dx.doi.org/10.1017/s1462399403007087.

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Brain injury following cerebral ischaemia (stroke) involves a complex combination of pathological processes, including excitotoxicity and inflammation leading to necrotic and apoptotic forms of cell death. At the cellular level, excitotoxicity is mediated by glutamate and its cognate receptors, resulting in increased intracellular calcium and free radical production, and eventual cell death. Recent evidence suggests that scaffolding molecules that associate with glutamate receptors at the postsynaptic density allow coupling of receptor activity to specific second messengers capable of mediatin

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29

Du, Rui, Ping Wang та Ning Tian. "CD3ζ-Mediated Signaling Protects Retinal Ganglion Cells in Glutamate Excitotoxicity of the Retina". Cells 13, № 12 (2024): 1006. http://dx.doi.org/10.3390/cells13121006.

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Excessive levels of glutamate activity could potentially damage and kill neurons. Glutamate excitotoxicity is thought to play a critical role in many CNS and retinal diseases. Accordingly, glutamate excitotoxicity has been used as a model to study neuronal diseases. Immune proteins, such as major histocompatibility complex (MHC) class I molecules and their receptors, play important roles in many neuronal diseases, while T-cell receptors (TCR) are the primary receptors of MHCI. We previously showed that a critical component of TCR, CD3ζ, is expressed by mouse retinal ganglion cells (RGCs). The

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30

Ivanova, Svetlana A., and Anton J. M. Loonen. "Levodopa-Induced Dyskinesia Is Related to Indirect Pathway Medium Spiny Neuron Excitotoxicity: A Hypothesis Based on an Unexpected Finding." Parkinson's Disease 2016 (2016): 1–5. http://dx.doi.org/10.1155/2016/6461907.

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A serendipitous pharmacogenetic finding links the vulnerability to developing levodopa-induced dyskinesia to the age of onset of Huntington’s disease. Huntington’s disease is caused by a polyglutamate expansion of the protein huntingtin. Aberrant huntingtin is less capable of binding to a member of membrane-associated guanylate kinase family (MAGUKs): postsynaptic density- (PSD-) 95. This leaves more PSD-95 available to stabilize NR2B subunit carrying NMDA receptors in the synaptic membrane. This results in increased excitotoxicity for which particularly striatal medium spiny neurons from the

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31

Kim, Gyung W., Jean-Christophe Copin, Makoto Kawase, et al. "Excitotoxicity is Required for Induction of Oxidative Stress and Apoptosis in Mouse Striatum by the Mitochondrial Toxin, 3-Nitropropionic Acid." Journal of Cerebral Blood Flow & Metabolism 20, no. 1 (2000): 119–29. http://dx.doi.org/10.1097/00004647-200001000-00016.

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Excitotoxicity is implicated in the pathogenesis of several neurologic diseases, such as chronic neurodegenerative diseases and stroke. Recently, it was reported that excitotoxicity has a relationship to apoptotic neuronal death, and that the mitochondrial toxin, 3-nitropropionic acid (3-NP), could induce apoptosis in the striatum. Although striatal lesions produced by 3-NP could develop through an excitotoxic mechanism, the exact relationship between apoptosis induction and excitotoxicity after 3-NP treatment is still not clear. The authors investigated the role of excitotoxicity and oxidativ

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32

Paiva, Bruna S., Diogo Neves, Diogo Tomé, et al. "Neuroprotection by Mitochondrial NAD Against Glutamate-Induced Excitotoxicity." Cells 14, no. 8 (2025): 582. https://doi.org/10.3390/cells14080582.

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Excitotoxicity is a pathological process that occurs in many neurological diseases, such as stroke or epilepsy, and is characterized by the extracellular accumulation of high concentrations of glutamate or other excitatory amino acids (EAAs). Nicotinamide adenine dinucleotide (NAD) depletion is an early event following excitotoxicity in many in vitro and in vivo excitotoxic-related models and contributes to the deregulation of energy homeostasis. However, the interplay between glutamate excitotoxicity and the NAD biosynthetic pathway is not fully understood. To address this question, we used a

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33

Han, Jin-Yi, Sun-Young Ahn, Eun-Hye Oh, et al. "Red Ginseng Extract Attenuates Kainate-Induced Excitotoxicity by Antioxidative Effects." Evidence-Based Complementary and Alternative Medicine 2012 (2012): 1–10. http://dx.doi.org/10.1155/2012/479016.

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This study investigated the neuroprotective activity of red ginseng extract (RGE,Panax ginseng, C. A. Meyer) against kainic acid- (KA-) induced excitotoxicityin vitroandin vivo. In hippocampal cells, RGE inhibited KA-induced excitotoxicity in a dose-dependent manner as measured by the MTT assay. To study the possible mechanisms of the RGE-mediated neuroprotective effect against KA-induced cytotoxicity, we examined the levels of intracellular reactive oxygen species (ROS) and [Ca2+]iin cultured hippocampal neurons and found that RGE treatment dose-dependently inhibited intracellular ROS and [Ca

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34

Martorell-Riera, Alejandro, Marc Segarra-Mondejar, Juan P. Muñoz, et al. "Mfn2 downregulation in excitotoxicity causes mitochondrial dysfunction and delayed neuronal death." Embo Journal 33, no. 20 (2014): 2388–407. https://doi.org/10.15252/embj.201488327.

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Mitochondrial fusion and fission is a dynamic process critical for the maintenance of mitochondrial function and cell viability. During excitotoxicity neuronal mitochondria are fragmented, but the mechanism underlying this process is poorly understood. Here, we show that Mfn2 is the only member of the mitochondrial fusion/fission machinery whose expression is reduced in in vitro and in vivo models of excitotoxicity. Whereas in cortical primary cultures, Drp1 recruitment to mitochondria plays a primordial role in mitochondrial fragmentation in an early phase that can be reversed once the insult

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35

Chao, Hsiao-Ming, Ing-Ling Chen, and Jorn-Hon Liu. "S-Allyl L-Cysteine Protects the Retina Against Kainate Excitotoxicity in the Rat." American Journal of Chinese Medicine 42, no. 03 (2014): 693–708. http://dx.doi.org/10.1142/s0192415x14500451.

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Excitotoxicity has been proposed to play a pivotal role in retinal ischemia. Retinal ischemia-associated ocular disorders are vision threatening. The aim was to also examine whether and how S-allyl L-cysteine (SAC) can protect the retina against kainate excitotoxicity. In vivo retinal excitotoxicity was induced by an intravitreous injection of 100 μM kainate into a Wistar rat eye for 1 day. The management and mechanisms involved in the processes were evaluated by electrophysiology, immunohistochemistry, histopathology, and various biochemical approaches. In the present study, the cultured reti

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36

Lu, Cheng-Wei, Chia-Chan Wu, Kuan-Ming Chiu, Ming-Yi Lee, Tzu-Yu Lin, and Su-Jane Wang. "Inhibition of Synaptic Glutamate Exocytosis and Prevention of Glutamate Neurotoxicity by Eupatilin from Artemisia argyi in the Rat Cortex." International Journal of Molecular Sciences 23, no. 21 (2022): 13406. http://dx.doi.org/10.3390/ijms232113406.

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The inhibition of synaptic glutamate release to maintain glutamate homeostasis contributes to the alleviation of neuronal cell injury, and accumulating evidence suggests that natural products can repress glutamate levels and associated excitotoxicity. In this study, we investigated whether eupatilin, a constituent of Artemisia argyi, affected glutamate release in rat cortical nerve terminals (synaptosomes). Additionally, we evaluated the effect of eupatilin in an animal model of kainic acid (KA) excitotoxicity, particularly on the levels of glutamate and N-methyl-D-aspartate (NMDA) receptor su

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37

Riche, Kade, and Natalie R. Lenard. "Quercetin’s Effects on Glutamate Cytotoxicity." Molecules 27, no. 21 (2022): 7620. http://dx.doi.org/10.3390/molecules27217620.

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The potentially therapeutic effects of the naturally abundant plant flavonoid quercetin have been extensively studied. An extensive body of literature suggests that quercetin’s powerful antioxidant effects may relate to its ability to treat disease. Glutamate excitotoxicity occurs when a neuron is overstimulated by the neurotransmitter glutamate and causes dysregulation of intracellular calcium concentrations. Quercetin has been shown to be preventative against many forms of neuronal cell death resulting from glutamate excitotoxicity, such as oncosis, intrinsic apoptosis, mitochondrial permeab

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Mironova, Yu S., I. A. Zhukova, N. G. Zhukova, V. M. Alifirova, O. P. Izhboldina, and A. V. Latypova. "Parkinson's disease and glutamate excitotoxicity." Zhurnal nevrologii i psikhiatrii im. S.S. Korsakova 118, no. 6 (2018): 50. http://dx.doi.org/10.17116/jnevro201811806250.

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Ong, Wei-Yi, Kazuhiro Tanaka, Gavin S. Dawe, Lars M. Ittner, and Akhlaq A. Farooqui. "Slow Excitotoxicity in Alzheimer's Disease." Journal of Alzheimer's Disease 35, no. 4 (2013): 643–68. http://dx.doi.org/10.3233/jad-121990.

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Huang, Chin-Wei, Ming-Chi Lai, Juei-Tang Cheng, Jing-Jane Tsai, Chao-Ching Huang, and Sheng-Nan Wu. "Pregabalin Attenuates Excitotoxicity in Diabetes." PLoS ONE 8, no. 6 (2013): e65154. http://dx.doi.org/10.1371/journal.pone.0065154.

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Jones, Rachel. "Blocking the pathway to excitotoxicity." Nature Reviews Neuroscience 3, no. 12 (2002): 916. http://dx.doi.org/10.1038/nrn992.

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Dubinsky, J. M. "EXCITOTOXICITY AS A STOCHASTIC PROCESS." Clinical and Experimental Pharmacology and Physiology 22, no. 4 (1995): 297–98. http://dx.doi.org/10.1111/j.1440-1681.1995.tb02001.x.

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McEntee, William J. "Wernicke's Encephalopathy: an Excitotoxicity Hypothesis." Metabolic Brain Disease 12, no. 3 (1997): 183–92. http://dx.doi.org/10.1023/b:mebr.0000007099.18010.72.

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Nilsen, Jon, Alison Morales, and Roberta Diaz Brinton. "Medroxyprogesterone acetate exacerbates glutamate excitotoxicity." Gynecological Endocrinology 22, no. 7 (2006): 355–61. http://dx.doi.org/10.1080/09513590600863337.

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Zhou, Xianju, Zhuoyou Chen, Wenwei Yun, Jianhua Ren, Chengwei Li, and Hongbing Wang. "Extrasynaptic NMDA Receptor in Excitotoxicity." Neuroscientist 21, no. 4 (2014): 337–44. http://dx.doi.org/10.1177/1073858414548724.

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Olney, J. "Excitotoxicity, apoptosis and neuropsychiatric disorders." Current Opinion in Pharmacology 3, no. 1 (2003): 101–9. http://dx.doi.org/10.1016/s1471489202000024.

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OLNEY, J. "Excitotoxicity, apoptosis and neuropsychiatric disorders." Current Opinion in Pharmacology 3, no. 1 (2003): 101–9. http://dx.doi.org/10.1016/s1471-4892(02)00002-4.

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Nicholls, David G., and Samantha L. Budd. "Mitochondria and neuronal glutamate excitotoxicity." Biochimica et Biophysica Acta (BBA) - Bioenergetics 1366, no. 1-2 (1998): 97–112. http://dx.doi.org/10.1016/s0005-2728(98)00123-6.

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Ludolph, A. C., M. Riepe, and K. Ullrich. "Excitotoxicity, energy metabolism and neurodegeneration." Journal of Inherited Metabolic Disease 16, no. 4 (1993): 716–23. http://dx.doi.org/10.1007/bf00711903.

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Johnston, Michael V. "Excitotoxicity in Perinatal Brain Injury." Brain Pathology 15, no. 3 (2006): 234–40. http://dx.doi.org/10.1111/j.1750-3639.2005.tb00526.x.

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