Protein Information

ID 376
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…

Compound Information

ID 615
Name sodium azide
CAS sodium azide

Reference

PubMed Abstract RScore(About this table)
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.
The features of neuronal damage induced by the mitochondrial toxin NaN (3) were investigated in rat primary cortical neuron cultures. Cell viability (MTT colorimetric determination) and transmembrane mitochondrial potential (J-C1 fluorescence) were concentration-dependently reduced 24 h after NaN (3); neither nuclear fragmentation by DAPI, nor Annexin V positivity by flow cytometry were detected, ruling out the occurrence of apoptosis. The loss in cell viability (to 54 +/- 2%) observed 24 h after a 10-min treatment with 3 mM NaN (3) was prevented by the NMDA glutamate receptor antagonist MK801 (1 microM), by the antioxidants trolox (100 microM) and acetyl-L-carnitine (1 mM) and by the nitric oxide synthase inhibitor, L-NAME (100 microM), but not by the guanylylcyclase inhibitor ODQ, 10 microM. The mitochondrial dysfunction induced by NaN (3) provides a common platform for investigating the mechanisms of both ischemic and degenerative neuronal injury, useful for screening potential protective agents against neuronal death.
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