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Biological Activity for ω-Conotoxin GVIA
ω-Conotoxin GVIA is a peptide neurotoxin; selectively and reversibly blocks N-type calcium channels (IC50 = 0.15 nM). Reduces (RS)-3,5-DHPG (Cat. No. 0342)-induced long term depression in vivo.
Technical Data for ω-Conotoxin GVIA
(Modifications: X = Hyp, Disulfide bridge between 1 - 16, 8 - 19, 15 - 26, Tyr-27 = C-terminal amide)
|Storage||Desiccate at -20°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
Solubility Data for ω-Conotoxin GVIA
|Solubility||Soluble to 1 mg/ml in water|
Product Datasheets for ω-Conotoxin GVIA
References for ω-Conotoxin GVIA
References are publications that support the biological activity of the product.
Tsien et al (1988) Multiple types of neuronal calcium channels and their selective modulation. TiNS 11 431 PMID: 2469160
Wright and Angu (1997) Prolonged cardiovascular effects of the N-type Ca2+ channel antagonist ω-conotoxin GVIA in conscious rabbits. J.Cardiovasc.Pharmacol. 30 392 PMID: 9300325
Connelly et al (2011) Distinct mechanisms contribute to agonist and synaptically induced metabotropic glutamate receptor long-term depression. Eur.J.Pharmacol. 667 160 PMID: 21575629
Sato et al (1993) Role of basic residues for the binding of omega-conotoxin GVIA to N-type calcium channels. Biochem.Biophys.Res.Comm. 194 1292 PMID: 8394704
If you know of a relevant reference for ω-Conotoxin GVIA, please let us know.
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Keywords: w-Conotoxin GVIA, w-Conotoxin GVIA supplier, Ca2+, channel, blockers, N-type, Calcium, CaV, Channels, voltage-gated, voltage-dependent, omega-Conotoxin, ω-conotoxin, GVIA, neurotoxins, venoms, Cav2.x, 1085, Tocris Bioscience
15 Citations for ω-Conotoxin GVIA
Citations are publications that use Tocris products. Selected citations for ω-Conotoxin GVIA include:
Perissinotti et al (2015) Calcium current homeostasis and synaptic deficits in hippocampal neurons from Kelch-like 1 knockout mice. Proc Natl Acad Sci U S A 8 444 PMID: 25610372
Smith et al (2013) Comparative functional expression of nAChR subtypes in rodent DRG neurons. Front Cell Neurosci 7 225 PMID: 24348328
Grubb and Burrone (2010) Activity-dependent relocation of the axon initial segment fine-tunes neuronal excitability. J Pharmacol Exp Ther 465 1070 PMID: 20543823
Chang (2010) Dynamic modulation of phasic and asynchronous glutamate release in hippocampal synapses. J Neurophysiol 103 392 PMID: 19889850
Haeberle et al (2004) Molecular profiling reveals synaptic release machinery in Merkel cells. Proc Natl Acad Sci U S A 101 14503 PMID: 15448211
Izzo et al (2012) Inhibitory effect of cannabichromene, a major non-psychotropic cannabinoid extracted from Cannabis sativa, on inflammation-induced hypermotility in mice. Br J Pharmacol 166 1444 PMID: 22300105
Bellono (2017) Molecular basis of ancestral vertebrate electroreception. Nature 543 391 PMID: 28264196
Pan et al (2014) σ-1 receptor antagonism restores injury-induced decrease of voltage-gated Ca2+ current in sensory neurons. Addict Biol 350 290 PMID: 24891452
Mahler et al (2014) Modafinil attenuates reinstatement of cocaine seeking: role for cystine-glutamate exchange and metabotropic glutamate receptors. J Neurosci 19 49 PMID: 23017017
Szabó et al (2014) Presynaptic calcium channel inhibition underlies CB1 cannabinoid receptor-mediated suppression of GABA release. PLoS One 34 7958 PMID: 24899717
Chu et al (2009) Secr. as a neurohypophysial factor regulating body water homeostasis. PLoS One 106 15961 PMID: 19805236
Schuwald et al (2013) Lavender oil-potent anxiolytic properties via modulating voltage dependent calcium channels. J Neurosci 8 e59998 PMID: 23637742
Medrihan et al (2013) Synapsin II desynchronizes neurotransmitter release at inhibitory synapses by interacting with presynaptic calcium channels. Nature 4 1512 PMID: 23443540
Cassilly et al (2016) SB-224289 Antagonizes the Antifungal Mechanism of the Marine Depsipeptide Papuamide A. Front Cell Neurosci 11 e0154932 PMID: 27183222
Kim and Alger (2010) Reduction in endocannabinoid tone is a homeostatic mechanism for specific inhibitory synapses. Nat Neurosci 13 592 PMID: 20348918
Do you know of a great paper that uses ω-Conotoxin GVIA from Tocris? Please let us know.
Reviews for ω-Conotoxin GVIA
Average Rating: 4.7 (Based on 3 Reviews.)
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The following concentrations we were used:1 μM Bay K, 10 μM nifedipine, 10 μM nimodipine, 300 nM omega -agatoxin, 1 μM omega -conotoxin, 5 μM mibefradil, 1 μM tetrodotoxin, 1 μM charybdotoxin, 100 nM iberiotoxin, 10 μM NS11021.
Biologically active compounds that have been documented to interact with awide range of targets including SB-224289 (Cat. # 1221), MG-624 (Cat.# 1356), GVIA (Cat. No. 1085), DPAT hydrobromide (Cat. No. 1080) and valinomycin (VA; Cat. # 3373) were ordered from Tocris Bioscience
Experiment to test dependence of field EPSPs in neural tissue from N-type Ca2+ channels. 10 min incubation with 25 microM omega -Conotoxin GVIA decreased significantly fEPSP amplitude. Blue: control. Red: after incubation with omega -Conotoxin GVIA.
Literature in this Area
Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* your copy today!
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