| Name | NMDA receptors (protein family or complex) |
|---|---|
| Synonyms | Glutamate [NMDA] receptor; Glutamate [NMDA] receptors; N methyl D aspartate receptor; N methyl D aspartate receptors; NMDA receptor; NMDA receptors |
| Name | rotenone |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 7666176 | Marey-Semper I, Gelman M, Levi-Strauss M: A selective toxicity toward cultured mesencephalic dopaminergic neurons is induced by the synergistic effects of energetic metabolism impairment and NMDA receptor activation. J Neurosci. 1995 Sep;15(9):5912-8. This selective toxic effect of on rotenone-pretreated dopaminergic neurons was blocked by either AMPA or NMDA receptor antagonists and mimicked by combined treatment with AMPA and or by alone when the medium was deprived of Mg2+ ions. |
32(0,1,1,2) | Details |
| 19428506 | Wu YN, Johnson SW: Rotenone reduces Mg2+-dependent block of currents in substantia nigra neurons. Neurotoxicology. 2009 Mar;30(2):320-5. Epub 2009 Jan 21. Moreover, we report that the kinase inhibitor blocked the ability of rotenone to augment NMDA receptor currents. |
31(0,1,1,1) | Details |
| 15910763 | Grammatopoulos TN, Ahmadi F, Jones SM, Fariss MW, Weyhenmeyer JA, Zawada WM: Angiotensin II protects cultured midbrain dopaminergic neurons against rotenone-induced cell death. Brain Res. 2005 May 31;1045(1-2):64-71. Epub 2005 Apr 26. Furthermore, both the NMDA receptor antagonist, MK801, and the antioxidant, alpha-tocopheryl analogue), prevented rotenone-induced toxicity. |
31(0,1,1,1) | Details |
| 10989660 | Greenamyre JT, MacKenzie G, Peng TI, Stephans SE: Mitochondrial dysfunction in Parkinson's disease. Biochem Soc Symp. 1999;66:85-97. Moreover, the facilitation of NMDA-receptor function leads to further mitochondrial dysfunction. We developed a novel model of PD in which chronic, systemic infusion of rotenone, a complex-I inhibitor, selectively kills dopaminergic nerve terminals and causes retrograde degeneration of substantia nigra neurons over a period of months. |
4(0,0,0,4) | Details |
| 9852565 | Castilho RF, Hansson O, Ward MW, Budd SL, Nicholls DG: Mitochondrial control of acute excitotoxicity in cultured cerebellar granule cells. J Neurosci. 1998 Dec 15;18(24):10277-86. A decreased initial [Ca2+] c elevation in cells whose mitochondria are depolarized by inhibition of the ATP synthase and respiratory chain (conditions which avoid ATP depletion) was attributed to enhanced Ca2+ extrusion from the cell rather than inhibited Ca2+ entry via the NMDA receptor. |
2(0,0,0,2) | Details |
| 11152381 | Kannurpatti SS, Joshi PG, Joshi NB: sequestering ability of mitochondria modulates influx of through glutamate receptor channel. Neurochem Res. 2000 Dec;25(12):1527-36. Combined treatment with oligomycin and rotenone further diminished the [Ca2+] i response and also abolished the CCCP mediated rise in [Ca2+] i. The rapid increase in [Ca2+] i was mainly due to influx of Ca2+ through the (NMDA) receptor channels. |
2(0,0,0,2) | Details |
| 2687018 | Skaper SD, Facci L, Milani D, Leon A: Monosialoganglioside protects against anoxia-induced neuronal death in vitro. Exp Neurol. 1989 Dec;106(3):297-305. Cells between 10 and 12 days in vitro were placed into an anoxic atmosphere or subjected to a chemical model of anoxia by a pulse exposure to rotenone. This neuronal injury was abolished by the specific N-methyl-D-aspartate receptor noncompetitive antagonists Mg2+, phencyclidine and MK-801, suggesting that this subtype of glutamate receptor is involved in the pathogenesis of anoxic granule cell injury. |
1(0,0,0,1) | Details |
| 8815895 | Schinder AF, Olson EC, Spitzer NC, Montal M: Mitochondrial dysfunction is a primary event in neurotoxicity. J Neurosci. 1996 Oct 1;16(19):6125-33. Sustained activation of NMDA receptors (20 min) elicits reversible elevation of [Ca2+] i. |
1(0,0,0,1) | Details |
| 7472402 | Dugan LL, Sensi SL, Canzoniero LM, Handran SD, Rothman SM, Lin TS, Goldberg MP, Choi DW: Mitochondrial production of reactive species in cortical neurons following exposure to J Neurosci. 1995 Oct;15(10):6377-88. The increased production of ROS was blocked by inhibitors of mitochondrial electron transport, rotenone or antimycin, and mimicked by the electron transport uncoupler, carbonyl p-trifluoromethoxyphenylhydrazone. These data support the possibility that NMDA receptor-mediated, Ca (2+)-dependent uncoupling of neuronal mitochondrial electron transport may contribute to the oxidative stress initiated by exposure. |
1(0,0,0,1) | Details |
| 9714760 | Nicholls DG, Budd SL: Mitochondria and neuronal excitotoxicity. Biochim Biophys Acta. 1998 Aug 10;1366(1-2):97-112. The response of cultured cerebellar granule cells to continuous exposure is characterised by a transient elevation in cytoplasmic free concentration followed by decay to a plateau as NMDA receptors partially inactivate. However, mitochondrial depolarisation (and hence inhibition of mitochondrial accumulation) without parallel ATP depletion (oligomycin plus either rotenone or antimycin A) strongly protects the cells against DCD. |
1(0,0,0,1) | Details |
| 9804614 | Leist M, Volbracht C, Fava E, Nicotera P: 1-Methyl-4-phenylpyridinium induces autocrine excitotoxicity, protease activation, and neuronal apoptosis. Mol Pharmacol. 1998 Nov;54(5):789-801. The neurotoxin 1-methyl-4-phenylpyridinium (MPP+) and other mitochondrial inhibitors (e.g., rotenone or 3-nitropropionic acid) elicited apoptosis in cerebellar granule cell cultures via stimulation of autocrine excitotoxicity. Cell death, increase in intracellular Ca2+ concentration, release of cytochrome c, and all biochemical and morphological signs of apoptosis were prevented by blockade of the N-methyl-D-aspartate receptor with noncompetitive, -site or -site inhibitors. |
1(0,0,0,1) | Details |
| 10098841 | Castilho RF, Ward MW, Nicholls DG: Oxidative stress, mitochondrial function, and acute excitotoxicity in cultured cerebellar granule cells. J Neurochem. 1999 Apr;72(4):1394-401. Mitochondrial depolarization by rotenone/oligomycin before addition is strongly neuroprotective, and the indication is therefore that mitochondrial Ca2+ loading leads to a delayed loss of bioenergetic function culminating in DCD and cell death. An inverse correlation is observed between the cytoplasmic free Ca2+ maintained in individual cells in the presence of and the ability of these cells to restore basal Ca2+ when NMDA receptors are inhibited and mitochondrial Ca2+ is released. |
1(0,0,0,1) | Details |
| 9742143 | Carriedo SG, Yin HZ, Sensi SL, Weiss JH: Rapid Ca2+ entry through Ca2+-permeable AMPA/Kainate channels triggers marked intracellular Ca2+ rises and consequent radical production. J Neurosci. 1998 Oct 1;18(19):7727-38. Thus, as with NMDA receptor activation, rapid Ca2+ influx through Ca2+-permeable AMPA/kainate channels also may result in mitochondrial Ca2+ overload and consequent injurious radical production. Inhibition of mitochondrial electron transport with CN- or rotenone almost completely blocked kainate-triggered radical production. |
1(0,0,0,1) | Details |
| 17673201 | Tozzi A, Costa C, Di Filippo M, Tantucci M, Siliquini S, Belcastro V, Parnetti L, Picconi B, Calabresi P: Memantine reduces neuronal dysfunctions triggered by in vitro ischemia and 3-nitropropionic acid. Exp Neurol. 2007 Oct;207(2):218-26. Epub 2007 Jun 29. Memantine, a low-affinity uncompetitive NMDA receptor antagonist, has been widely utilized for the treatment of Alzheimer's disease. Moreover, memantine showed protection against irreversible field potential loss induced by 3-nitropropionic acid (3-NP), an inhibitor of the mitochondrial complex II, without influencing toxicity induced by rotenone, a complex I inhibitor. |
1(0,0,0,1) | Details |
| 7777208 | Blandini F, Porter RH, Greenamyre JT: Autoradiographic study of mitochondrial complex I and glutamate receptors in the basal ganglia of rats after unilateral subthalamic lesion. Neurosci Lett. 1995 Feb 17;186(2-3):99-102. The unexpected decrease in [3H] MK-801 binding in SNr may be related to presynaptic NMDA receptor modifications. |
1(0,0,0,1) | Details |
| 17947304 | Duan Y, Gross RA, Sheu SS: Ca2+-dependent generation of mitochondrial reactive species serves as a signal for poly (ADP- polymerase-1 activation during excitotoxicity. J Physiol. 2007 Dec 15;585(Pt 3):741-58. Epub 2007 Oct 18. Based on the spatial profile of -induced ROS generation, we found that only mitochondria showed a significant ROS increase within 30 min after NMDA receptor activation. This ROS increase was inhibited by the mitochondrial complex inhibitors rotenone and oligomycin, but not by the cytosolic phospholipase A (2) or xanthine oxidase inhibitors. |
1(0,0,0,1) | Details |
| 19076430 | Nicholls DG: Oxidative stress and energy crises in neuronal dysfunction. Ann N Y Acad Sci. 2008 Dec;1147:53-60. and entering via the N-methyl-D-aspartate receptor impose a large energetic load on cells and can use the entire respiratory capacity of the in situ mitochondria. As a result, even modest restrictions in mitochondrial capacity -- caused by low concentrations of electron transport chain inhibitors such as rotenone, as in models of Parkinson's disease; low concentrations of uncouplers, to test the so-called neuroprotective mild uncoupling hypothesis; or preexisting oxidative stress -- greatly potentiate excitotoxicity. |
1(0,0,0,1) | Details |
| 16919272 | Centonze D, Prosperetti C, Barone I, Rossi S, Picconi B, Tscherter A, De Chiara V, Bernardi G, Calabresi P: NR2B-containing NMDA receptors promote the effects of 3-nitropropionic acid but not of rotenone in the striatum. Exp Neurol. 2006 Dec;202(2):470-9. Epub 2006 Aug 17. We also found that blockade of a subset of NMDA receptors containing the NR2B subunit was sufficient to protect the striatum from the injurious effects of 3-NP, an effect unrelated to the prevention of membrane excitation by NMDA receptor stimulation. |
1(0,0,0,1) | Details |
| 8931459 | Budd SL, Nicholls DG: Mitochondria, regulation, and acute excitotoxicity in cultured cerebellar granule cells. J Neurochem. 1996 Dec;67(6):2282-91. -evoked Ca2+ deregulation is exacerbated by the mitochondrial respiratory chain inhibitor rotenone. It is concluded that mitochondrial Ca2+ accumulation is a necessary intermediate in excitotoxicity, whereas the decreased Ca2+ flux into cells with depolarized mitochondria may reflect a feedback inhibition of the NMDA receptor mediated by localized Ca2+ accumulation in a microdomain accessible to the mitochondria. |
1(0,0,0,1) | Details |
| 7561883 | Sabri MI, Lystrup B, Roy DN, Spencer PS: Action of beta-N-oxalylamino- on mouse brain NADH-dehydrogenase activity. J Neurochem. 1995 Oct;65(4):1842-8. beta-N-Oxalylamino- (L-BOAA), a non-protein neuroexcitatory amino acid present in the seeds of Lathyrus sativus (chickling or grass pea), is known to produce its effects by overstimulation of non-N-methyl-D-aspartate receptors, especially alpha-amino-3--5-methylisoxazole-4- (AMPA) receptors, at micromolar concentrations. Two known inhibitors (rotenone and 1-methyl-4-phenylpyridinium ion, MPP+) of this mitochondrial enzyme produced significant inhibition under identical conditions. |
1(0,0,0,1) | Details |
| 11245674 | Rego AC, Ward MW, Nicholls DG: Mitochondria control ampa/kainate receptor-induced cytoplasmic deregulation in rat cerebellar granule cells. J Neurosci. 2001 Mar 15;21(6):1893-901. Although mitochondria mediate the delayed failure of cytoplasmic Ca (2+) homeostasis [delayed Ca (2+) deregulation (DCD)] in rat cerebellar granule cells resulting from chronic activation of NMDA receptors, their role in AMPA/KA-induced DCD remains to be established. In contrast to -evoked DCD, no additional protection was afforded by the further addition of rotenone. |
1(0,0,0,1) | Details |
| 17611283 | Yadava N, Nicholls DG: Spare respiratory capacity rather than oxidative stress regulates excitotoxicity after partial respiratory inhibition of mitochondrial complex I with rotenone. J Neurosci. 2007 Jul 4;27(27):7310-7. activation of NMDA receptors used the full respiratory capacity of the in situ mitochondria, and > 80% of the -stimulated respiration was attributable to increased cellular ATP demand. |
1(0,0,0,1) | Details |
| 17560718 | Wu YN, Johnson SW: Rotenone potentiates currents in substantia nigra neurons. . Neurosci Lett. 2007 Jun 27;421(2):96-100. Epub 2007 May 24. |
0(0,0,0,0) | Details |
| 15223368 | Kanki R, Nakamizo T, Yamashita H, Kihara T, Sawada H, Uemura K, Kawamata J, Shibasaki H, Akaike A, Shimohama S: Effects of mitochondrial dysfunction on glutamate receptor-mediated neurotoxicity in cultured rat spinal motor neurons. Brain Res. 2004 Jul 23;1015(1-2):73-81. We investigated the relationship between excitotoxicity and mitochondrial dysfunction elicited by rotenone (a complex I inhibitor), (a complex II inhibitor), or antimycin (a complex III inhibitor), in primary cultures of the embryonic rat spinal cord. |
0(0,0,0,0) | Details |
| 15255947 | Vesce S, Kirk L, Nicholls DG: Relationships between levels and delayed deregulation in cultured cerebellar granule cells exposed continuously to J Neurochem. 2004 Aug;90(3):683-93. Oxidative stress of mitochondrial origin is readily detectable, as the inhibitors rotenone and antimycin A markedly increase levels with no effect on cytoplasmic-free Ca2+. |
0(0,0,0,0) | Details |