| Name | glutamate receptors (protein family or complex) |
|---|---|
| Synonyms | Glutamate receptor; Glutamate receptors |
| Name | rotenone |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 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. stimulation in the absence of Ca2+ in the extracellular medium elicited a small transient rise in [Ca2+] i which can be attributed to the mobilization of Ca2+ from IP3 sensitive endoplasmic reticulum pools consequent to activation of metabotropic glutamate receptors. |
1(0,0,0,1) | Details |
| 9449429 | Nakao N, Nakai K, Itakura T: Metabolic inhibition enhances selective toxicity of toward mesencephalic neurons in vitro. Brain Res. 1997 Nov 28;777(1-2):202-9. We investigated whether metabolic inhibition with rotenone, an inhibitor of complex I of the mitochondrial respiratory chain, may enhance the toxicity of toward DA neurons in mesencephalic cultures. |
0(0,0,0,0) | 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. |
112(1,2,2,2) | 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. Our results suggest that oxidative stress releases followed by activation of postsynaptic ionotropic glutamate receptors that trigger production and results in a flood of NA from cytoplasmic stores. 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 |
| 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. Since activation of the glutamate receptors can induce increased levels of reactive species (ROS), we investigated the relationship of mitochondrial Ca (2+) uptake and ROS generation, and the possibility that ROS increase is a required signal for PARP-1 activation in cultured striatal neurons. 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 |
| 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. neurotoxicity is triggered primarily by massive Ca2+ influx arising from overstimulation of the subtype of glutamate receptors. |
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. |
1(0,0,0,1) | Details |