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興奮毒性

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出典 ^ a b “Impairment of mitochondrial calcium handling in a mtSOD1 cell culture model of motoneuron disease”. BMC Neurosci 10: 64. (2009). doi:10.1186/1471-2202-10-64. PMC 2716351. .mw-parser-output cite.citation{font-style:inherit;word-wrap:break-word}.mw-parser-output .citation q{quotes:"\"""\"""'""'"}.mw-parser-output .citation.cs-ja1 q,.mw-parser-output .citation.cs-ja2 q{quotes:"「""」""『""』"}.mw-parser-output .citation:target{background-color:rgba(0,127,255,0.133)}.mw-parser-output .id-lock-free a,.mw-parser-output .citation .cs1-lock-free a{background:url("//upload.wikimedia.org/wikipedia/commons/6/65/Lock-green.svg")right 0.1em center/9px no-repeat}.mw-parser-output .id-lock-limited a,.mw-parser-output .id-lock-registration a,.mw-parser-output .citation .cs1-lock-limited a,.mw-parser-output .citation .cs1-lock-registration a{background:url("//upload.wikimedia.org/wikipedia/commons/d/d6/Lock-gray-alt-2.svg")right 0.1em center/9px no-repeat}.mw-parser-output .id-lock-subscription a,.mw-parser-output .citation .cs1-lock-subscription a{background:url("//upload.wikimedia.org/wikipedia/commons/a/aa/Lock-red-alt-2.svg")right 0.1em center/9px no-repeat}.mw-parser-output .cs1-ws-icon a{background:url("//upload.wikimedia.org/wikipedia/commons/4/4c/Wikisource-logo.svg")right 0.1em center/12px no-repeat}.mw-parser-output .cs1-code{color:inherit;background:inherit;border:none;padding:inherit}.mw-parser-output .cs1-hidden-error{display:none;color:#d33}.mw-parser-output .cs1-visible-error{color:#d33}.mw-parser-output .cs1-maint{display:none;color:#3a3;margin-left:0.3em}.mw-parser-output .cs1-format{font-size:95%}.mw-parser-output .cs1-kern-left{padding-left:0.2em}.mw-parser-output .cs1-kern-right{padding-right:0.2em}.mw-parser-output .citation .mw-selflink{font-weight:inherit}PMID 19545440. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2716351/.
^ “Delayed increase of Ca2+ influx elicited by glutamate: role in neuronal death”. Molecular Pharmacology 36 (1): 106?112. (Jul 1989). PMID 2568579.
^ Zheng, Sika; Eacker, Stephen M.; Hong, Suk Jin; Gronostajski, Richard M.; Dawson, Ted M.; Dawson, Valina L. (July 2010). “NMDA-induced neuronal survival is mediated through nuclear factor I-A in mice”. The Journal of Clinical Investigation 120 (7): 2446?2456. doi:10.1172/JCI33144. ISSN 1558-8238. PMC 2898580. PMID 20516644. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2898580/.
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^ Camacho, A; Massieu, L (2006). “Role of glutamate transporters in the clearance and release of glutamate during ischemia and its relation to neuronal death.”. Archives of Medical Research 37 (1): 11?8. doi:10.1016/j.arcmed.2005.05.014. PMID 16314180.
^ Fujikawa, DG (2005). “Prolonged seizures and cellular injury: understanding the connection.”. Epilepsy & Behavior 7 Suppl 3: S3?11. doi:10.1016/j.yebeh.2005.08.003. PMID 16278099.
^ Watkins, Jeffrey C; Jane, David E (2 February 2009). “The glutamate story”. British Journal of Pharmacology 147 (S1): S100?S108. doi:10.1038/sj.bjp.0706444. PMC 1760733. PMID 16402093. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1760733/.
^ Lucas, DR; Newhouse, JP (1957). “The toxic effect of sodium L-glutamate on the inner layers of the retina.”. Archives of Ophthalmology 58 (2): 193?201. doi:10.1001/archopht.1957.00940010205006. PMID 13443577.
^ Olney, JW (1969). “Brain lesions, obesity, and other disturbances in mice treated with monosodium glutamate.”. Science 164 (3880): 719?21. Bibcode: 1969Sci...164..719O. doi:10.1126/science.164.3880.719. hdl:10217/207298. PMID 5778021.
^ Hardingham, G. E.; Fukunaga, Y.; Bading, H. (May 2002). “Extrasynaptic NMDARs oppose synaptic NMDARs by triggering CREB shut-off and cell death pathways”. Nature Neuroscience 5 (5): 405?414. doi:10.1038/nn835. ISSN 1097-6256. PMID 11953750. https://pubmed.ncbi.nlm.nih.gov/11953750.
^ Yan, Jing; Bengtson, C. Peter; Buchthal, Bettina; Hagenston, Anna M.; Bading, Hilmar (9 October 2020). “Coupling of NMDA receptors and TRPM4 guides discovery of unconventional neuroprotectants”. Science 370 (6513). doi:10.1126/science.aay3302. ISSN 1095-9203. PMID 33033186. https://pubmed.ncbi.nlm.nih.gov/33033186.
^ Head trauma : basic, preclinical, and clinical directions. Leonard P. Miller, Ronald L. Hayes, Jennifer K. Newcomb. New York: Wiley-Liss. (2001). pp. 87-113. ISBN 0-471-36015-5. OCLC 45618924. https://www.worldcat.org/oclc/45618924
^ Clements, JD; Lester, RA; Tong, G; Jahr, CE; Westbrook, GL (1992). “The time course of glutamate in the synaptic cleft”. Science 258 (5087): 1498?501. Bibcode: 1992Sci...258.1498C. doi:10.1126/science.1359647. PMID 1359647.
^ Yang Derek D. (October 1997). “Absence of excitotoxicity-induced apoptosis in the hippocampus of mice lacking the Jnk3 gene”. Nature 389 (6653): 865?870. Bibcode: 1997Natur.389..865Y. doi:10.1038/39899. PMID 9349820.
^ Ankarcrona Maria (October 1995). “Glutamate-induced neuronal death: A succession of necrosis or apoptosis depending on mitochondrial function”. Neuron 15 (4): 961?973. doi:10.1016/0896-6273(95)90186-8. PMID 7576644.
^ Hulsebosch (Apr 2009). “Mechanisms of chronic central neuropathic pain after spinal cord injury”. Brain Res Rev 60 (1): 202?13. doi:10.1016/j.brainresrev.2008.12.010. PMC 2796975. PMID 19154757. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2796975/.
^ Nakamura (Aug 2010). “S-nitrosylation of Drp1 links excessive mitochondrial fission to neuronal injury in neurodegeneration”. Mitochondrion 10 (5): 573?8. doi:10.1016/j.mito.2010.04.007. PMC 2918703. PMID 20447471. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2918703/.
^ a b Dutta (Jan 2011). “Mechanisms of neuronal dysfunction and degeneration in multiple sclerosis”. Prog Neurobiol 93 (1): 1?12. doi:10.1016/j.pneurobio.2010.09.005. PMC 3030928. PMID 20946934. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3030928/.
^ Stavrovskaya, IG; Kristal, BS (2005). “The powerhouse takes control of the cell: is the mitochondrial permeability transition a viable therapeutic target against neuronal dysfunction and death?”. Free Radical Biology & Medicine 38 (6): 687?97. doi:10.1016/j.freeradbiomed.2004.11.032. PMID 15721979.
^ Allen, J; Romay-Tallon, R; Brymer, K; Caruncho, H; Kalynchuk, L (2018). “Mitochondria and Mood: Mitochondrial Dysfunction as a Key Player in the Manifestation of Depression”. Frontiers in Neuroscience 12: 386. doi:10.3389/fnins.2018.00386. PMC 5997778. PMID 29928190. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5997778/.
^ Li (2001). “Na+-K+-ATPase inhibition and depolarization induce glutamate release via reverse Na+-dependent transport in spinal cord white matter”. Neuroscience 107 (4): 675?683. doi:10.1016/s0306-4522(01)00385-2. PMID 11720790.

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出典: フリー百科事典『ウィキペディア（Wikipedia）』
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