ω conotoxin mviic

Manufactured by Alomone

Sourced in Israel, Palestine, State of

ω-conotoxin MVIIC is a peptide derived from the venom of the marine snail Conus magus. It functions as a selective and potent blocker of N-type calcium channels.

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3 protocols using ω conotoxin mviic

Botulinum Neurotoxin Activation and Reagents

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BoNT/A1 (2.5 × 10⁸ MLD₅₀/mg), BoNT/D1 (2.8 × 10⁷ MLD₅₀/mg) and BoNT/E1 (3.0 × 10⁷ MLD₅₀/mg) were purchased from Metabiologics (Madison, WI, USA). For BoNT/E, toxin was activated by a 60 min incubation at 37 °C with 0.3 mg/mL TPCK-treated trypsin in 0.05 M sodium phosphate buffer (pH 6.5)^{19 (link)}. ω-agatoxin IVA, ω-conotoxin MVIIC and GV-58 were purchased from Alomone Labs (Jerusalem, Israel). FPL 64176 was purchased from Tocris Bioscience (Bristol, UK). All reagents for electrophysiology buffers were obtained from Sigma-Aldrich (St. Louis, MO, USA).

Beske P.H., Hoffman K.M., Machamer J.B., Eisen M.R, & McNutt P.M. (2017). Use-dependent potentiation of voltage-gated calcium channels rescues neurotransmission in nerve terminals intoxicated by botulinum neurotoxin serotype A. Scientific Reports, 7, 15862.

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Pharmacological Toolkit for Neuroscience

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Diltiazem-HCl (100 mM in distilled H₂O [dH₂O]), D-AP5 (50 mM in dH₂O), lidocaine (100 mM in DMSO), (S)-(-)-Bay K 8644 (50 mM in DMSO), TTA-P2 (10 mM in DMSO), verapamil-HCl (100 mM in dH₂O), ω-conotoxin GVIA (1 mM in dH₂O), ω-conotoxin MVIIC (300 µM in dH₂O), and ω-agatoxin IV A (200 µM in dH₂O) were from Alomone Laboratories and dissolved as indicated in parentheses. AIP (500 µM in dH₂O), H-89 dihydrochloride (10 mM in DMSO), and U0126 (50 mM in DMSO) were from Calbiochem. IBMX (100 mM in DMSO), 5-HT (10 mM in dH₂O), fentanyl (10 mM in dH₂O), NB001 (75 mM in dH₂O), NKY80 (100 mM in DMSO), and oxycodone hydrochloride (10 mM in dH₂O) were from Sigma-Aldrich. FK 506 (50 mM in DMSO), forskolin (10 mM in DMSO), ionomycin calcium salt (10 mM in DMSO), KN-92 (10 mM in DMSO), KN-93 (10 mM in DMSO), [Leu⁵]-enkephalin (1 mM in 0.1% BSA in dH₂O), SQ22536 (50 mM in DMSO), and ST 034307 (50 mM in DMSO) were from Tocris. Rp-cAMPS-pAB and 4-ABnOH (10 mM in DMSO) were synthesized and provided by F. Schwede (BioLog, Bremen, Germany).

Isensee J., van Cann M., Despang P., Araldi D., Moeller K., Petersen J., Schmidtko A., Matthes J., Levine J.D, & Hucho T. (2021). Depolarization induces nociceptor sensitization by CaV1.2-mediated PKA-II activation. The Journal of Cell Biology, 220(10), e202002083.

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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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