| Name | NMDA receptor (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 | sodium azide |
|---|---|
| CAS | sodium azide |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 15680257 | Katsuki H, Shinohara A, Fujimoto S, Kume T, Akaike A: Tetraethylammonium exacerbates ischemic neuronal injury in rat cerebrocortical slice cultures. Eur J Pharmacol. 2005 Jan 31;508(1-3):85-91. Epub 2005 Jan 6. Exposure of cultures to -free conditioning solution containing sodium azide and 2-deoxyglucose caused neuronal cell death as assessed by cellular uptake of propidium iodide, which was prevented by MK-801, an (NMDA) receptor antagonist. |
32(0,1,1,2) | Details |
| 11978402 | Grammatopoulos T, Morris K, Ferguson P, Weyhenmeyer J: Angiotensin protects cortical neurons from hypoxic-induced apoptosis via the angiotensin type 2 receptor. Brain Res Mol Brain Res. 2002 Mar 28;99(2):114-24. The (NMDA) receptor antagonist MK-801 blocked sodium azide-induced cell death suggesting that the NMDA receptor contributes to the mediated cell death. |
31(0,1,1,1) | Details |
| 12445574 | Kume T, Nishikawa H, Taguchi R, Hashino A, Katsuki H, Kaneko S, Minami M, Satoh M, Akaike A: Antagonism of NMDA receptors by sigma receptor ligands attenuates chemical ischemia-induced neuronal death in vitro. Eur J Pharmacol. 2002 Nov 29;455(2-3):91-100. The induction of chemical ischemia by sodium azide and 2-deoxy- led to delayed neuronal death in a time- and concentration-dependent manner, as determined by trypan blue exclusion. |
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. Results show that neuronal damage can be efficiently prevented in the presence of and the (NMDA) receptor antagonist MK-801, whereas the non-NMDA receptor antagonist NBQX, and PBN showed partial protection. |
1(0,0,0,1) | Details |
| 9313890 | Smith TS, Bennett JP Jr: Mitochondrial toxins in models of neurodegenerative diseases. Brain Res. 1997 Aug 15;765(2):183-8. These results support the concept of developing free radical scavengers for both AD and PD and further suggest that inhibition of NOS and blockade of NMDA receptor function may alter progression of idiopathic PD. In brain microdialysis in awake rats, striatal 'OH output increased 3-5-fold after infusion of methylpyridinium ion (MPP+), a complex I inhibitor, or sodium azide, a complex IV inhibitor. |
1(0,0,0,1) | Details |
| 16135390 | Cavallini S, Marti M, Marino S, Selvatici R, Beani L, Bianchi C, Siniscalchi A: Effects of chemical ischemia in cerebral cortex slices. Neurochem Int. 2005 Dec;47(7):482-90. Superfused rat cerebral cortex slices were submitted to a continuous electrical (5 Hz) stimulation and treated with sodium azide (1-10 mM) in the presence of 2 mM 2-deoxyglucose ("chemical ischemia"). After restoring normal superfusion conditions, release recovered to 70+/-3.1% of the controls; the N-methyl-D-aspartate receptor antagonist MK-801 (10 microM) as well as the scavengers, haemoglobin (20 microM) and 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-l-oxyl-3-oxide (150 microM), improved the recovery in presynaptic activity, showing that both and play detrimental roles in chemical ischemia. |
1(0,0,0,1) | Details |
| 17384288 | Siniscalchi A, Cavallini S, Marino S, Falzarano S, Franceschetti L, Selvatici R: Effects of chemical ischemia on cerebral cortex slices: focus on mitogen-activated protein kinase cascade. Ann N Y Acad Sci. 2006 Dec;1090:445-54. All CI/REP-induced effects were prevented by the NMDA receptor antagonist MK-801, 10 microM, suggesting the involvement of In superfused, electrically stimulated rat cerebral cortex slices, chemical ischemia (CI) was induced by a 5-min treatment with the mitochondrial toxin, sodium azide (10 mM), combined with the glycolysis blocker, 2-deoxyglucose (2 mM). |
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. This indicated that NMDA receptors were being activated, causing some of the observed toxicity. |
1(0,0,0,1) | Details |
| 10613517 | Knyihar-Csillik E, Okuno E, Vecsei L: Effects of in vivo sodium azide administration on the immunohistochemical localization of aminotransferase in the rat brain. Neuroscience. 1999;94(1):269-77. The chemical hypoxia induced by mitochondrial toxins produces a secondary excitotoxicity, leading to the activation of N-methyl-D-aspartate receptors. |
1(0,0,0,1) | Details |
| 15683745 | Gabra BH, Afify EA, Daabees TT, Abou Zeit-Har MS: The role of the NO/ pathways in the development of morphine withdrawal induced by naloxone in vitro. Pharmacol Res. 2005 Apr;51(4):319-27. In addition, the NO precursor (5x10 (-4) M) as well as the NO donors sodium nitroprusside (SNP; 1 microM) and sodium azide (NaZ; 10 microM) were able to revert the effect of L-NAME returning the amplitude of naloxone-induced contracture to the same level in control morphine-dependent ilea. We also demonstrated that the competitive NMDA receptor antagonist DL-2-amino-5-phosphonovaleric acid (AP-5; 50 microM) potently reduced the amplitude of naloxone-induced contracture in the same model, an effect that was reversed by co-administration of the excitatory amino acid (40 microM). |
1(0,0,0,1) | Details |
| 10340744 | Jorgensen NK, Petersen SF, Damgaard I, Schousboe A, Hoffmann EK: Increases in [Ca2+] i and changes in intracellular pH during chemical anoxia in mouse neocortical neurons in primary culture. J Neurosci Res. 1999 May 15;56(4):358-70. A change in pHo (8.2 or 6.6), or addition of and non-NMDA receptor antagonists (D-AP5 and CNQX) in combination, significantly reduced the increase in [Ca2+] i, pointing to a protective effect of extracellular alkalosis or acidosis, and involvement of excitatory amino acids. |
1(0,0,0,1) | 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. All the above effects depended on release and consequent NMDA receptor activation, since the antagonist MK-801 (1 microM) prevented them, and the spontaneous efflux of [(3) H]-d-aspartate from superfused neurons was concentration-dependently increased by NaN (3). |
1(0,0,0,1) | Details |
| 16988055 | Katnik C, Guerrero WR, Pennypacker KR, Herrera Y, Cuevas J: Sigma-1 receptor activation prevents intracellular dysregulation in cortical neurons during in vitro ischemia. J Pharmacol Exp Ther. 2006 Dec;319(3):1355-65. Epub 2006 Sep 20. The sigma receptor agonist, 1,3-di-o-tolyl- (DTG), was shown to depress [Ca (2+)](i) elevations observed in response to ischemia induced by sodium azide and deprivation. |
0(0,0,0,0) | Details |