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ω conotoxin gvia

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ω-conotoxin GVIA is a peptide derived from the venom of the marine cone snail Conus geographus. It functions as a selective and potent blocker of N-type voltage-gated calcium channels.

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Lab products found in correlation

Nifedipine, by Merck Group (4 mentions) ω agatoxin iva, by Merck Group (4 mentions) Tetrodotoxin, by Merck Group (3 mentions) Veratridine, by Merck Group (2 mentions) Flunarizine, by Merck Group (2 mentions) Anti hb9, by Developmental Studies Hybridoma Bank (2 mentions) Sulpiride, by Merck Group (2 mentions) Quinpirole, by Merck Group (2 mentions) Citalopram, by Merck Group (1 mentions) Scopolamine, by Bio-Techne (1 mentions) Cadmium chloride, by Merck Group (1 mentions) Bay k8644, by Merck Group (1 mentions) Tetrodotoxin ttx, by Bio-Techne (1 mentions) Nimodipine, by Merck Group (1 mentions) Dihydro β erythroidine dhβe, by Bio-Techne (1 mentions) Cyclopiazonic acid cpa, by Bio-Techne (1 mentions) ω conotoxin mviic, by Alomone (1 mentions) Picrotoxin, by Merck Group (1 mentions) Lidocaine n ethyl bromide qx 314, by Merck Group (1 mentions) ω conotoxin mviic, by Merck Group (1 mentions)

9 protocols using ω conotoxin gvia

1

Modulating Spinal Cord Ca2+ Dynamics

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Spontaneous Ca2+ activity in the developing spinal cord was modified using both pharmacological and genetic approaches. For pharmacological manipulation of spontaneous Ca2+ activity, agarose beads impregnated with 1 mM veratridine (voltage-gated Na+ channel agonist, Sigma) or a cocktail of voltage-gated Ca2+ and Na+ channel blockers (VGCblock; 200 nM calcicludine (Calbiochem), 10 μM ω-conotoxin–GVIA, 10 μM flunarizine, and 10 μg/ml tetrodotoxin (Sigma)) were implanted at stage 17-18. For genetic manipulation of spontaneous Ca2+ activity, rNav2aαβ (Nav2a, 100 pg rNav2aα and 500 pg rNav2aβ mRNA) was bilaterally injected at the two-cell stage. Embryos were grown at room temperature until stage 35–36 when samples were collected and processed for immunostaining with anti-HB9 (Developmental Studies Hybridoma Bank) as described above in Immunostaining. Immunoreactive cells were counted in at least 20 consecutive sections per larva, and from at least 4 larvae per treatment.
Spencer K.A., Belgacem Y.H., Visina O., Shim S., Genus H, & Borodinsky L.N. (2019). Growth at Cold Temperature Increases the Number of Motor Neurons to Optimize Locomotor Function. Current biology : CB, 29(11), 1787-1799.e5.
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2

Preparation of Calcium Channel Blockers

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ω-conotoxin GVIA (C9915) was purchased from Sigma-Aldrich and dissolved in phosphate buffered saline (PBS; pH 7.4). Nifedipine (481981) was purchased from Calbiochem and was dissolved in DMSO.
Pitake S., Middleton L.J., Abdus-Saboor I, & Mishra S.K. (2019). Inflammation Induced Sensory Nerve Growth and Pain Hypersensitivity Requires the N-Type Calcium Channel Cav2.2. Frontiers in Neuroscience, 13, 1009.
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3

Neuropharmacological Compound Preparation

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Cadmium chloride, ω-conotoxin GVIA (CTX), ω-agatoxin IVA (ATX), tetrodotoxin (TTX), Bay K 8644, nifedipine, quinpirole, sulpiride, CP-93,129, (2R)-amino-5-phosphonovaleric acid (APV), 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo[f]quinoxaline-2,3-dione (NBXQ), picrotoxin and citalopram were obtained from Sigma-Aldrich. Oxotremorine-m (OXO-M), dihydro-β-erythroidine (DHβE), and scopolamine were obtained from Tocris Cookson. Drugs were dissolved as stock solutions in water or DMSO and aliquoted and frozen at −20°C before use. Each of the drugs was diluted in aCSF immediately before each experiment. When used, the final concentration of DMSO external solution was always <0.05%.
Sgobio C., Kupferschmidt D.A., Cui G., Sun L., Li Z., Cai H, & Lovinger D.M. (2014). Optogenetic Measurement of Presynaptic Calcium Transients Using Conditional Genetically Encoded Calcium Indicator Expression in Dopaminergic Neurons. PLoS ONE, 9(10), e111749.
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4

Voltage-Gated Channel Modulation

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The treatment began 30 min prior to electrical stimulation, and continued throughout the stimulation. Each drug was added to both stimulated and unstimulated cultures. Tetrodotoxin (TTX; 3 mM stock in citrate buffer, pH=4.8; Tocris Bioscience, Ellisville, MO), ω-conotoxin GVIA (50 μM stock in PBS; Sigma), and nimodipine (10 mM stock in ethanol; Sigma), were used at final concentrations of 1.5 μM, 1 μM, and 2 μM, respectively.
Vermehren-Schmaedick A., Khanjian R.A, & Balkowiec A. (2015). CELLULAR MECHANISMS OF ACTIVITY-DEPENDENT BDNF EXPRESSION IN PRIMARY SENSORY NEURONS. Neuroscience, 310, 665-673.
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5

Modulating Spinal Cord Ca2+ Dynamics

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Spontaneous Ca2+ activity in the developing spinal cord was modified using both pharmacological and genetic approaches. For pharmacological manipulation of spontaneous Ca2+ activity, agarose beads impregnated with 1 mM veratridine (voltage-gated Na+ channel agonist, Sigma) or a cocktail of voltage-gated Ca2+ and Na+ channel blockers (VGCblock; 200 nM calcicludine (Calbiochem), 10 μM ω-conotoxin–GVIA, 10 μM flunarizine, and 10 μg/ml tetrodotoxin (Sigma)) were implanted at stage 17-18. For genetic manipulation of spontaneous Ca2+ activity, rNav2aαβ (Nav2a, 100 pg rNav2aα and 500 pg rNav2aβ mRNA) was bilaterally injected at the two-cell stage. Embryos were grown at room temperature until stage 35–36 when samples were collected and processed for immunostaining with anti-HB9 (Developmental Studies Hybridoma Bank) as described above in Immunostaining. Immunoreactive cells were counted in at least 20 consecutive sections per larva, and from at least 4 larvae per treatment.
Spencer K.A., Belgacem Y.H., Visina O., Shim S., Genus H, & Borodinsky L.N. (2019). Growth at Cold Temperature Increases the Number of Motor Neurons to Optimize Locomotor Function. Current biology : CB, 29(11), 1787-1799.e5.
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6

Pharmacological Agents for Neurophysiology

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ω-conotoxin GVIA (CTX), ω-agatoxin IVA (ATX), nifedipine, quinpirole and sulpiride, were obtained from Sigma-Aldrich. (1S, 2S)-2-[2-[[3-(1H-Benzimidazol-2-yl) propyl] methylamino]ethyl]-6-fluoro- 1, 2, 3, 4-tetrahydro-1-(1-methylethyl)-2-naphthalenyl cyclopropanecarboxylate dihydrochloride (NNC 50-0396), Cyclopiazonic acid (CPA) and dihydro-β-erythroidine (DHβE) were obtained from Tocris Cookson. Drugs were dissolved as stock solutions in water or DMSO and aliquoted and frozen at −20 °C before use. Each of the drugs was diluted in aCSF immediately before each experiment. When used, the final concentration of DMSO external solution was always <0.05%.
Sgobio C., Sun L., Ding J., Herms J., Lovinger D.M, & Cai H. (2019). Unbalanced calcium channel activity underlies selective vulnerability of nigrostriatal dopaminergic terminals in Parkinsonian mice. Scientific Reports, 9, 4857.
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7

Intrathecal Injection of Neurotoxins in Mice

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ω-conotoxin GVIA (Sigma-Aldrich U.S.A.), ω-conotoxin MVIIC (Alomone Labs, Jerusalem, Israel), and ω-agatoxin IVA (Sigma-Aldrich U.S.A.) were dissolved in sterile saline. Nifedipine (Sigma-Aldrich U.S.A.) was first dissolved in a stock solution of 10 mM with 50% DMSO in saline. This was further diluted to the appropriate testing dilutions with saline to a final DMSO concentration <0.0001%, which did not affect the behavioral sensitivity of animals (data not shown). These drug solutions were injected intrathecally (5 µL/mouse) between lumbar regions L4–L5 via a 30-gauge, 1/2-inch needle attached to a microinjector (Tritech Research Inc, Los Angeles, CA) (Inoue et al., 2004 (link)). In the case that mice were used for repetitive injections, a drug-free period of at least 48 hours after the last drug injection was introduced. Molarity of injected drugs was calculated based on estimated 40 µL mouse cerebrospinal fluid (Johanson et al., 2008 (link)).
Chang E., Chen X., Kim M., Gong N., Bhatia S, & Luo Z.D. (2014). Differential Effects of Voltage-Gated Calcium Channel Blockers on Calcium Channel Alpha-2-Delta-1 Subunit Protein Mediated Nociception. European journal of pain (London, England), 19(5), 639-648.
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8

Pharmacological Toolkit for Neuroscience Research

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2,3-Dioxo-6-nitro-1,2,3,4-tetrahydrobenzo[f]quinoxaline-7-sulfonamide (NBQX), D-(−)-2-Amino-5-phosphonopentanoic acid (AP5), strychnine, picrotoxin, tetraethylammonium (TEA), 4-aminopyradine (4-AP), tetrodotoxin (TTX), nifedipine, ω-conotoxin GVIA, ω-conotoxin MVIIC, lidocaine N-ethyl bromide (QX-314), was obtained from Sigma Aldrich (St. Louis, MO, USA). TTX, nifedipine, ω-conotoxin GVIA, ω-conotoxin MVIIC, QX-314, and nickel were prepared as 1000X stock solutions. nifedipine, and QX-314 were prepared in DMSO. TTX was prepared in water. Stock solutions of ω-conotoxin GVIA and ω-conotoxin MVIIC were prepared in deoxygenated solution containing 0.1% BSA, 100 mM NaCl, 10 mM Trizma, and 1 mM EDTA, pH 7.5. Drugs were then diluted to working concentrations directly preceding experiments. TTA-P2 was obtained from Alomone Labs.
Nigam A., Hargus N.J., Barker B.S., Ottolini M., Hounshell J.A., Bertram EH I.I.I., Perez-Reyes E, & Patel M.K. (2019). Inhibition of T-Type Calcium Channels in mEC Layer II Stellate Neurons Reduces Neuronal Hyperexcitability Associated with Epilepsy.. Epilepsy research, 154, 132-138.
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9

Preparation of Neuroscience Compounds

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TTX, 2,3-dihydroxy-6-nitro-7-sulfamoylbenzo(f)-quinox aline (NBQX), DL-2-amino-5-phosphonopentanoic acid (AP5), ω-Conotoxin GVIA, ω-agatoxin IVA and LY379268 were prepared in distilled H 2 O. Baclofen was prepared in 0.5% acetic acid. CGP55845, LY341495, nifedipine and ryanodine were prepared in DMSO. All drugs were diluted to their final concentrations in aCSF (final DMSO concentrations were ࣘ0.1%). TTX and AP5 were purchased from Abcam (Cambridge, MA, USA). ω-Conotoxin GVIA and ω-agatoxin IVA were purchased from Sigma-Aldrich (St Louis, MO, USA). All other drugs were purchased from Tocris Bioscience (Ellisville, MO, USA).
Kupferschmidt D.A, & Lovinger D.M. (2015). Inhibition of presynaptic calcium transients in cortical inputs to the dorsolateral striatum by metabotropic GABA(B) and mGlu2/3 receptors. The Journal of physiology, 593(10).
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