ω-Conotoxin GVIA
(Synonyms: Ω-芋螺毒素) 目录号 : GC13886
ω-芋螺毒素 GVIA 是 N 型 Ca2+ 通道的抑制剂。
Cas No.:106375-28-4
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
| Cell experiment [1]: | |
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Cell lines |
Rat pituitary melanotropic cells |
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Preparation Method |
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Reaction Conditions |
1 or 10 µM |
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Applications |
1 µM ω-Conotoxin GVIA blocked the high voltage-activated current by 25.5±3.6%. The block at 10µM ω-Conotoxin GVIA was 22.9±2.5% (not significantly different from the block by 1µM;n = 3), indicating thatω-Conotoxin GVIA yields a saturating effect. |
| Animal experiment [2]: | |
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Animal models |
male COBS CD (SD) rats |
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Preparation Method |
In these animals the intravenous administration of graded doses of ω-Conotoxin GVIA (1--2 nmol/kg) |
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Dosage form |
Intravenous injection, 1--2 nmol/kg |
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Applications |
Intravenous injection caused a progressive loss of tension development of tibialis muscle indirectly evoked by the electrical stimulation of the sciatic nerve, ω-Conotoxin GVIA (1 nmol/kg i.v.) reduced the strength of muscle contraction by 75% in about 27 min (from |
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References: [1]: H.D. Mansvelder, J.C. Stoof, K.S. Kits. Dihydropyridine block of ω-agatoxin IVA- and ω-conotoxin GVIA-sensitive Ca2+ channels in rat pituitary melanotropic cells.Eur. J. Pharmacol., 311 (1996), pp. 293-304 | |
ω-Conotoxin GVIA is a cone snail toxin that selectively blocks N-type channels in neurons [1].
ω-Conotoxin GVIA binds to human neocortical, rat hippocampal, and chick brain synaptic plasma membranes (IC50s = 4.6, 60, and 150 pM, respectively, in radioligand binding assays) [3,4,5].
ω-Conotoxin GVIA markedly reduced the amplitude of the tetanic contractions of the tibialis anterior muscle in mice, but tetanic facilitation was not impaired. The muscle contractions elicited by direct electrical stimulation were not significantly modified by ω-Conotoxin GVIA. ω-Conotoxin GVIA did not had any significant changes in systemic blood pressure [5].
References:
[1]. H.D. Mansvelder, J.C. Stoof, K.S. Kits. Dihydropyridine block of ω-agatoxin IVA- and ω-conotoxin GVIA-sensitive Ca2+ channels in rat pituitary melanotropic cells.Eur. J. Pharmacol., 311 (1996), pp. 293-304
[2]. Feuerstein, T.J., Dooley, D.J., and Seeger, W. Inhibition of norepinephrine and acetylcholine release from human neocortex by ω-conotoxin GVIA. J. Pharmacol. Exp. Ther. 252(2), 778-785 (1990).
[3]. Lampe, R.A., Lo, M.M., Keith, R.A., et al. Effects of site-specific acetylation on ω-conotoxin GVIA binding and function. Biochemistry 32(13), 3255-3260 (1993).
[4]. Sato, K., Park, N.G., Kohno, T., et al. Role of basic residues for the binding of ω-conotoxin GVIA to N-type calcium channels. Biochem. Biophys. Res. Commun. 194(3), 1292-1296 (1993).
[5]: Rossoni G, Berti F, La Maestra L, Clementi F. ω-Conotoxin GVIA binds to and blocks rat neuromuscular junction. Neuroscience Letters. 1994;176:185-188.
ω-芋螺毒素 GVIA 是一种锥形蜗牛毒素，可选择性地阻断神经元中的 N 型通道[1]。
ω-芋螺毒素 GVIA 与人类新皮质、大鼠海马和鸡脑突触质膜结合（在放射性配体结合试验中，IC50 分别 = 4.6、60 和 150 pM）[3,4,5].
ω-芋螺毒素 GVIA 显着降低了小鼠胫骨前肌的强直收缩幅度，但强直易化作用并未受损。 ω-芋螺毒素 GVIA 未显着改变由直接电刺激引起的肌肉收缩。 ω-芋螺毒素 GVIA 对体循环血压无明显影响[5]。
| Cas No. | 106375-28-4 | SDF | |
| 别名 | Ω-芋螺毒素 | ||
| Canonical SMILES | C[C@](O)([H])[C@@](/N=C(O)/[C@](/N=C(O)/[C@]1([H])C[C@](O)([H])CN12)([H])CC3=CC=C(O)C=C3)([H])/C(O)=N/[C@@](/C(O)=N/[C@@](/C(O)=N\[C@@](/C(O)=N\[C@@](C(O)=N)([H])CC4=CC=C(O)C=C4)([H])CSSC[C@@](N=C(O)[C@](N=C(O)[C@](N=C(O)[C@](N=C(O)[C@](N=C(O)[C@]5([H])C[ | ||
| 分子式 | C120H182N38O43S6 | 分子量 | 3037.35 |
| 溶解度 | Soluble to 1 mg/ml in Water | 储存条件 | Desiccate at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 0.3292 mL | 1.6462 mL | 3.2923 mL |
| 5 mM | 0.0658 mL | 0.3292 mL | 0.6585 mL |
| 10 mM | 0.0329 mL | 0.1646 mL | 0.3292 mL |
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动物平均体重 | g | |
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动物数量 | 只 |
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ω-Conotoxin GVIA mimetics that bind and inhibit neuronal Ca(v)2.2 ion channels
Mar Drugs2012 Oct;10(10):2349-2368.PMID: 23170089DOI: 10.3390/md10102349
The neuronal voltage-gated N-type calcium channel (Ca(v)2.2) is a validated target for the treatment of neuropathic pain. A small library of anthranilamide-derived ω-Conotoxin GVIA mimetics bearing the diphenylmethylpiperazine moiety were prepared and tested using three experimental measures of calcium channel blockade. These consisted of a ¹²⁵I-ω-Conotoxin GVIAdisplacement assay, a fluorescence-based calcium response assay with SH-SY5Y neuroblastoma cells, and a whole-cell patch clamp electrophysiology assay with HEK293 cells stably expressing human Ca(v)2.2 channels. A subset of compounds were active in all three assays. This is the first time that compounds designed to be mimics of ω-Conotoxin GVIA and found to be active in the ¹²⁵I-ω-Conotoxin GVIA displacement assay have also been shown to block functional ion channels in a dose-dependent manner.
Effects of omega-Conotoxin GVIA on cardiac sympathetic nerve function
J Auton Nerv Syst1998 Jan 19;68(1-2):43-8.PMID: 9531444DOI: 10.1016/s0165-1838(97)00120-3
Using a cardiac dialysis technique, the effects of omega-Conotoxin GVIA (N-type Ca2+ channel blocker) on cardiac sympathetic nerve function was examined in anesthetized cats. Dialysis probes were implanted in the left ventricular wall and the concentration of dialysate norepinephrine (NE) served as an indicator of NE output at cardiac sympathetic nerve endings. Administration of omega-Conotoxin GVIA (10 microg/kg i.v.) suppressed dialysate NE responses to the nerve stimulation. The ouabain (1 microM) induced NE increment was less markedly suppressed by omega-Conotoxin GVIA. Furthermore, omega-Conotoxin GVIA neither influenced neuronal NE uptake nor tyramine induced release of NE from stores. These findings suggest that the neuronal effect of omega-Conotoxin GVIA is attributable to a reduction of exocytotic NE release without alterations of neuronal NE uptake or storage. Cardiac dialysis with omega-Conotoxin GVIA offers a new approach for the discrimination between Ca2+ dependent exocytotic and non-exocytotic NE release.
Effects of omega-Conotoxin GVIA on autonomic neuroeffector transmission in various tissues
Br J Pharmacol1990 Oct;101(2):437-47.PMID: 2175236DOI: 10.1111/j.1476-5381.1990.tb12727.x
1. The effects of omega-Conotoxin GVIA (conotoxin), a potent inhibitor of neuronal N-type Ca2+ channels, have been examined on responses to stimulation of noradrenergic, cholinergic and non-adrenergic, non-cholinergic (NANC) nerves in a range of isolated tissues to investigate the role of conotoxin-sensitive Ca2+ channels in neurotransmission. 2. Contractions elicited by field stimulation of noradrenergic nerves in rat and mouse anococcygeus muscles, rabbit ear artery and rat vas deferens (epididymal portion) were inhibited by conotoxin. Responses to noradrenaline, and to adenosine triphosphate in the vas deferens, were not affected. 3. Positive chronotropic responses to field stimulation of noradrenergic nerves were inhibited by conotoxin in rat and mouse atria, but responses to noradrenaline and tyramine were not affected. 4. The stimulation-induced release of noradrenaline was inhibited by conotoxin in the rabbit ear artery and in rat and mouse atria. 5. Relaxations in response to stimulation of the noradrenergic perivascular mesenteric nerves were reduced or abolished by conotoxin in rat and rabbit jejunum. The response to noradrenaline in rat jejunum was not affected. 6. Contractions elicited by stimulation of cholinergic nerves were inhibited by conotoxin in rat jejunum and mouse ileum (perivascular mesenteric nerves), and in guinea-pig taenia caeci (field stimulation). Responses to acetylcholine in rat jejunum and mouse ileum were not affected. 7. Contractions elicited by stimulation of the cholinergic plus NANC pelvic nerves were inhibited by conotoxin in rabbit colon, and to a lesser extent in guinea-pig colon. The stimulation-induced contraction of the guinea-pig colon was inhibited by conotoxin by a greater proportion in the presence than in the absence of atropine. Responses to acetylcholine were not affected in the rabbit colon but were slightly reduced in the guinea-pig colon. 8. Relaxations in response to field stimulation of NANC nerves were inhibited by conotoxin in guinea-pig taenia caeci and rat gastric fundus strips, and in rat anococcygeus muscle when the tone was raised by guanethidine but not when it was raised by carbachol. The relaxations produced by sodium nitroprusside in the rat gastric fundus and anococcygeus were not affected. 9. Contractions of the rat bladder elicited by stimulation of the peri-urethral nerves, which are NANC- and cholinergically mediated, were relatively insensitive to inhibition by conotoxin. The response were almost completely abolished by tetrodotoxin. 10. The conotoxin-induced inhibitions of responses to nerve stimulation developed slowly and persisted after removal of conotoxin. The responses were almost completely abolished by tetrodotoxin. 10. The conotoxin-induced inhibitions of responses to nerve stimulation developed slowly and persisted after removal of conotoxin. 11. The inhibitory effect of conotoxin was inversely proportional to the frequency of stimulation (in several preparations) and to the Ca2+ concentration in the bathing solution (in rat vas deferens). These observations suggest that the inhibition by conotoxin of the Ca2+ influx required for excitation-secretion coupling in autonomic nerve terminals is not absolute, and can be overcome by repeated stimulation or by raising the Ca2 + concentration.
omega-Conotoxin GVIA disrupts memory formation in the day-old chick
Neurobiol Learn Mem1995 Nov;64(3):276-84.PMID: 8564381DOI: 10.1006/nlme.1995.0010
Calcium channel antagonists have previously been shown to alleviate age-associated reductions in memory acquisition and enhance retention for a number of different tasks. We have investigated the effects of pretraining injections of nifedipine, nimodipine, and amlodipine (L-type calcium channel antagonists) and omega-Conotoxin GVIA (an N-type calcium channel antagonist) on passive avoidance and visual discrimination learning in day-old Ross 1 chunky chicks. None of the L-type calcium channel antagonists at any time or dose tested caused amnesia for the passive avoidance task or enhanced weak learning, and nifedipine did not affect acquisition or retention of the visual discrimination task. However, pretraining bilateral intracerebral injections of 1.25 pmole/hemisphere omega-Conotoxin GVIA produced amnesia for the passive avoidance task in chicks tested 30 min or 3 h after training. The same dose of omega-Conotoxin GVIA significantly reduced the rate of acquisition of the visual discrimination task, but did not affect retention of the task when tested 30 min or 3 h after training. These data indicate that calcium uptake via presynaptic N-type omega-conotoxin-sensitive but not L-type dihydropyridine-sensitive calcium channels is necessary for memory formation in young chicks.