554412
Tetrodotoxin, Citrate, Fugu sp.
Sinónimos:
TTx
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About This Item
UNSPSC Code:
12352202
NACRES:
NA.51
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General description
Reversibly blocks Na+ channels, which are essential for the propagation of impulses in excitable membranes. Useful as a marker of Na+ channels in excitable tissues. Inhibits the release of glutamate via Na+-dependent glutamate transporter and prevents veratradine-induced intracellular Ca2+ accumulation (IC50 = 63 nM).
Reversibly blocks Na+ channels, which are essential for the propagation of impulses in excitable membranes. Useful as a marker of Na+ channels in excitable tissues. Inhibits the release of glutamate via Na+-dependent glutamate transporter and prevents veratradine-induced intracellular Ca2+ accumulation (IC50 = 63 nM).
Application
Tetrodotoxin, Fugu sp., CAS 18660-81-6, is a reversible blocker of Na+ channels. Inhibits the release of glutamate via Na+-dependent glutamate transporter.
Biochem/physiol Actions
Target IC50:63 nM Iinhibiting the release of glutamate via Na+-dependent glutamate transporter and prevents veratradine-induced intracellular Ca2+ accumulation
Physical form
Crystalline solid. Contains sodium citrate.
Reconstitution
Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 3 months at -20°C. Activity is destroyed if exposed to alkaline or strongly acidic conditions.
Other Notes
Not available for sale outside of the United States.
signalword
Danger
hcodes
Hazard Classifications
Acute Tox. 1 Oral
Storage Class
6.1A - Combustible acute toxic Cat. 1 and 2 / very toxic hazardous materials
wgk_germany
WGK 3
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M Nakamura et al.
Toxicon : official journal of the International Society on Toxinology, 23(2), 271-276 (1985-01-01)
Analysis of puffer fish tissue extracts by a fluorometric tetrodotoxin analyzer revealed the presence of three tetrodotoxin derivatives besides tetrodotoxin. The derivatives were isolated and identified as tetrodonic acid, 4-epitetrodotoxin and anhydrotetrodotoxin on the basis of mass spectral and 1H
P G Lysko et al.
Stroke, 25(12), 2476-2482 (1994-12-01)
Studies examining the role of tetrodotoxin-sensitive ion channels in hypoxic-ischemic neuronal damage have concluded that sodium influx is an important initiating event. We examined the neuroprotectant effect of tetrodotoxin on both cultured cerebellar neurons and on CA1 hippocampal neurons of
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