| Name | calcium channel (protein family or complex) |
|---|---|
| Synonyms | calcium channel |
| Name | sodium azide |
|---|---|
| CAS | sodium azide |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 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. These findings show that the predominant source of increase induced by NaN (3) is extracellular, involving glutamate receptor activation in a first step and calcium channel (mainly of the N-type) opening in a second step. |
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| 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"). |
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| 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. |
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| 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. |
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| 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. Sodium azide, a collision quencher of singlet reduced the magnitude of FALI-mediated effects supporting a role for reactive species in the process. |
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| 15545708 | Nunemaker CS, Satin LS: Comparison of metabolic oscillations from mouse pancreatic beta cells and islets. Endocrine. 2004 Oct;25(1):61-7. Depolarizing responses to the mitochondrial poison NaN3 were reduced in beta cells (35 +/- 4%) vs islets (58 +/- 9%), and hyperpolarizing responses to the calcium channel blocker nifedipine were enhanced in beta cells (15 +/- 4%) vs islets (8 +/- 1%), suggesting that mitochondria in dispersed beta cells were less energized than those in intact islets (p < 0.005), possibly due to elevated intracellular |
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