| Name | glutamate receptor |
|---|---|
| Synonyms | GRINL1A; GUP1; GUP2; GRINL1A combined protein; GRINL1A combined protein Gcom10; GRINL1A combined protein Gcom10 precursor; GRINL1A combined protein Gcom11; GRINL1A combined protein Gcom11 precursor… |
| Name | rotenone |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 18615648 | Schuh RA, Matthews CC, Fishman PS: Interaction of mitochondrial respiratory inhibitors and excitotoxins potentiates cell death in hippocampal slice cultures. J Neurosci Res. 2008 Nov 15;86(15):3306-13. In the present study, we determined whether concomitant exposure of rotenone plus tetraethylammonium (TEA) or the specific glutamate receptor agonists or alpha-amino-3--5-methyl-4-isoxazoleproprionic acid (AMPA) would cause greater cell death in organotypic hippocampal slice cultures than when given separately. |
31(0,1,1,1) | Details |
| 16624952 | Jiang Q, Yan Z, Feng J: Activation of group III metabotropic glutamate receptors attenuates rotenone toxicity on dopaminergic neurons through a microtubule-dependent mechanism. J Neurosci. 2006 Apr 19;26(16):4318-28. Here, we show that application of group III metabotropic glutamate receptor (mGluRIII) agonists (e.g., L-AP-4) significantly reduced rotenone toxicity on midbrain TH+ neurons in culture. |
31(0,1,1,1) | 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. |
3(0,0,0,3) | 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. |
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 |
| 14697328 | Bonsi P, Calabresi P, De Persis C, Papa M, Centonze D, Bernardi G, Pisani A: Early ionic and membrane potential changes caused by the pesticide rotenone in striatal cholinergic interneurons. Exp Neurol. 2004 Jan;185(1):169-81. Interestingly, ion and membrane potential changes were mimicked by ouabain, inhibitor of the Na+-K+ATPase, and were insensitive to tetrodotoxin (TTX) or to a combination of glutamate receptor antagonists. |
1(0,0,0,1) | Details |
| 10908611 | Luetjens CM, Bui NT, Sengpiel B, Munstermann G, Poppe M, Krohn AJ, Bauerbach E, Krieglstein J, Prehn JH: Delayed mitochondrial dysfunction in excitotoxic neuron death: cytochrome c release and a secondary increase in production. J Neurosci. 2000 Aug 1;20(15):5715-23. We monitored intracellular production of hippocampal neurons during and after exposure to the glutamate receptor agonist (300 microm). The secondary rise could be inhibited by the complex I inhibitor rotenone (in combination with oligomycin) and mimicked by the complex III inhibitor antimycin A. |
1(0,0,0,1) | Details |
| 10989660 | Greenamyre JT, MacKenzie G, Peng TI, Stephans SE: Mitochondrial dysfunction in Parkinson's disease. Biochem Soc Symp. 1999;66:85-97. 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. This relieves the voltage-dependent Mg2+ block of the subtype of the glutamate receptor, which is highly permeable to Ca2+. |
1(0,0,0,1) | Details |
| 12895517 | Milusheva E, Sperlagh B, Shikova L, Baranyi M, Tretter L, Adam-Vizi V, Vizi ES: Non-synaptic release of [3H] in response to oxidative stress combined with mitochondrial dysfunction in rat hippocampal slices. Neuroscience. 2003;120(3):771-81. It was also attenuated by the glutamate receptor antagonists 6-cyano-7-nitroquinoxaline-2,3-dione (30 microM) and (+/-)-2-amino-5-phosphonopentanoic acid (10 microM), by the synthase inhibitors, N omega-nitro- methyl ester (100 microM), or 7-nitroindazole (50 microM) and by the vesicular uptake inhibitor tetrabenazine (1 microM). Mitochondrial inhibitors, i.e. rotenone (10 microM), and oligomycin (10 microM) in combination, also decreased the energy charge, but they had only a mild effect on [(3) H] NA release. |
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 pathogenesis of several neurodegenerative diseases may involve indirect excitotoxic mechanisms, where glutamate receptor overstimulation is a secondary consequence of initial functional defects of neurons (e.g., impairment of mitochondrial energy generation). 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. |
1(0,0,0,1) | Details |
| 11299330 | Almeida A, Bolanos JP: A transient inhibition of mitochondrial ATP synthesis by synthase activation triggered apoptosis in primary cortical neurons. J Neurochem. 2001 Apr;77(2):676-90. From these results, we suggest that glutamate receptor-mediated NOS activation would trigger MPT pore opening and transient inhibition of ATP synthesis leading to apoptosis in a neuronal subpopulation, whereas other groups of neurons would undergo oxidative stress and persistent inhibition of ATP synthesis leading to necrosis. |
1(0,0,0,1) | Details |