| Name | SOD1 |
|---|---|
| Synonyms | ALS; ALS 1; ALS1; IPOA; Indophenoloxidase A; SOD; SOD 1; SOD1… |
| Name | strychnine |
|---|---|
| CAS | strychnidin-10-one |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 17284186 | Bories C, Amendola J, Lamotte d'Incamps B, Durand J: Early electrophysiological abnormalities in lumbar motoneurons in a transgenic mouse model of amyotrophic lateral sclerosis. Eur J Neurosci. 2007 Jan;25(2):451-9. Therefore, we investigated the electrical properties of lumbar motoneurons in an in-vitro neonatal spinal cord preparation isolated from SOD1 (G85R) mice, which is a transgenic model of amyotrophic lateral sclerosis. |
5(0,0,0,5) | Details |
| 15885796 | Raiteri L, Zappettini S, Stigliani S, Paluzzi S, Raiteri M, Bonanno G: release induced by activation of and transporters in spinal cord is enhanced in a mouse model of amyotrophic lateral sclerosis. Neurotoxicology. 2005 Oct;26(5):883-92. Potentiation of the spontaneous amino acid release is likely to be mediated by activation of a GLY or a GABA transporter, since the effect of GLY was counteracted by the GLY transporter blocker glycyldodecylamide but not by the GLY receptor antagonists strychnine and 5,7-dichlorokynurenate while the effect of was diminished by the GABA transporter blocker SKF89976-A but not by the GABA receptor antagonists SR9531 and CGP52432. We studied the release of [3H] d-aspartate ([3H] d-ASP) and endogenous evoked by (GLY) or from spinal cord synaptosomes in mice expressing a mutant form of human SOD1 with a Gly93Ala substitution ([SOD1-G93A (+)]), a transgenic model of amyotrophic lateral sclerosis, in mice expressing the non-mutated form of human SOD1 [SOD1+], and in non-transgenic littermates [SOD1 (-)/G93A (-)]. |
3(0,0,0,3) | Details |
| 12684256 | Raiteri L, Paolucci E, Prisco S, Raiteri M, Bonanno G: Activation of a transporter on spinal cord neurons causes enhanced release in a mouse model of amyotrophic lateral sclerosis. Br J Pharmacol. 2003 Mar;138(6):1021-5. The release of [(3) H] D-aspartate ([(3) H] D-ASP) or [(3) H] evoked by from spinal cord synaptosomes was compared in mice expressing mutant human SOD1 with a Gly (93) substitution ([SOD1-G93A (+)]), a transgenic model of amyotrophic lateral sclerosis, and in control mice. Potentiation of the spontaneous release of both amino acids is likely to be mediated by activation of a transporter, since the effects of were counteracted by the transporter blocker glycyldodecylamide but not by the glycine receptor antagonists strychnine and 5,7-dichlorokynurenate. |
2(0,0,0,2) | Details |