| 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 | sodium azide |
|---|---|
| CAS | sodium azide |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 8926628 | Varming T, Drejer J, Frandsen A, Schousboe A: Characterization of a chemical anoxia model in cerebellar granule neurons using sodium azide: protection by nifedipine and MK-801. J Neurosci Res. 1996 Apr 1;44(1):40-6. The viability of neuronal cultures after treatment with azide, with or without preincubation with calcium channel blockers, tetrodotoxin (TTX), or glutamate receptor antagonists, was monitored by subsequent incubation with the tetrazolium dye MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium followed by extraction and spectrophotometric quantification of cellularly reduced MTT. |
2(0,0,0,2) | Details |
| 17316809 | Marino S, Marani L, Nazzaro C, Beani L, Siniscalchi A: Mechanisms of sodium azide-induced changes in intracellular concentration in rat primary cortical neurons. Neurotoxicology. 2007 May;28(3):622-9. Epub 2007 Jan 20. In this study the questions of possible additional sources of influx, besides glutamate receptor activation, and of the time-course of NaN (3) effects have been addressed by measuring [Ca (2+)](i) in rat primary cortical cultures with the FURA-2 method. |
2(0,0,0,2) | Details |
| 11340649 | Garcia O, Massieu L: Strategies for neuroprotection against L-trans-2,4-pyrrolidine dicarboxylate-induced neuronal damage during energy impairment in vitro. J Neurosci Res. 2001 May 15;64(4):418-28. Results show that cerebellar granule neurons are not vulnerable to transient uptake inhibition by L-trans-pyrrolidine-2,4-dicarboxylate (PDC) despite the increase in the extracellular concentration of unless they are simultaneously exposed to the mitochondrial toxins 3-nitropropionic acid (3-NP) or sodium azide. The protective effect of alternative energy substrates, such as and against PDC-induced neuronal death during 3-NP exposure was studied and compared to the effects of the antioxidant the spin trapper alpha-phenyl-N-tert-butylnitrone (PBN), voltage-dependent calcium channel antagonists, and glutamate receptor antagonists. |
1(0,0,0,1) | Details |
| 16873413 | Guo J, Chen H, Puhl HL 3rd, Ikeda SR: Fluorophore-assisted light inactivation produces both targeted and collateral effects on N-type calcium channel modulation in rat sympathetic neurons. J Physiol. 2006 Oct 15;576(Pt 2):477-92. Epub 2006 Jul 27. Here we examine a novel FALI modality that utilizes a fluorescein-conjugated polypeptide, alpha-bungarotoxin (BTX) and a 13 amino acid BTX-binding site engineered into the N-terminus of metabotropic glutamate receptor 8a (mGluR8a), a class C G-protein-coupled receptor (GPCR). Sodium azide, a collision quencher of singlet reduced the magnitude of FALI-mediated effects supporting a role for reactive species in the process. |
1(0,0,0,1) | Details |
| 9676750 | Jensen JB, Schousboe A, Pickering DS: AMPA receptor mediated excitotoxicity in neocortical neurons is developmentally regulated and dependent upon receptor desensitization. Neurochem Int. 1998 May-Jun;32(5-6):505-13. In order to describe the pharmacology of AMPA-mediated toxicity, several glutamate receptor antagonists were used: MK-801, NS 394, NBQX, GYKI 52466, GYKI 53405 and GYKI 53655. |
1(0,0,0,1) | Details |
| 18841470 | Selvatici R, Previati M, Marino S, Marani L, Falzarano S, Lanzoni I, Siniscalchi A: Sodium azide induced neuronal damage in vitro: evidence for non-apoptotic cell death. Neurochem Res. 2009 May;34(5):909-16. Epub 2008 Oct 8. |
0(0,0,0,0) | Details |