ArticleBritish journal of pharmacology1996
Inhibition of neuromuscular transmission in the myenteric plexus of guinea-pig ileum by omega-conotoxins GVIA, MVIIA, MVIIC and SVIB.
Article in British journal of pharmacology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 19 citations in OpenAlex.
- Mechanisms of butylidenephthalide for twitch facilitation in electrically stimulated mouse vas deferens.Pharmaceutical biology · 2018Article
- Upregulation of L-type calcium channels in colonic inhibitory motoneurons of P/Q-type calcium channel-deficient mice.American journal of physiology. Gastrointestinal and liver physiology · 2016Article
- Lack of effect of Z-butylidenephthalide on presynaptic N-type Ca²⁺ channels in isolated guinea-pig ileum.Naunyn-Schmiedeberg's archives of pharmacology · 2016Article
- Calcium channel subtypes for cholinergic and nonadrenergic noncholinergic neurotransmission in isolated guinea pig trachea.Naunyn-Schmiedeberg's archives of pharmacology · 2010Article
- Role of N-type calcium channels in autonomic neurotransmission in guinea-pig isolated left atria.British journal of pharmacology · 1999Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. The effects of a number of Ca2+ channel blockers on the transmural electrical stimulation or receptor agonist-elicited contractile responses of guinea-pig ileum were compared. 2. omega-Conotoxins (MVIIA, GVIA, SVIB and MVIIC), but not omega-agatoxin IVA, completely blocked the twitch responses evoked by low frequency (0.1 Hz) transmural stimulation without inhibition of the contractures evoked by exogenous acetylcholine. The concentration-inhibition curves were shifted by changes of external Ca2+. 3. The tetanic contractures produced by a high frequency (30 Hz) train of stimulation were inhibited by omega-conotoxins by only 25-30%, except for omega-conotoxin MVIIC, which produced about 55% inhibition, all significantly less than that produced by atropine (about 70%) or tetrodotoxin (about 85%). Combinations of omega-conotoxins did not produce additive inhibitory effects. 4. The four omega-conotoxins as well as atropine produced similar partial inhibition (53-62%) of the contractures evoked by dimethylphenylpiperazinium, while tetrodotoxin inhibited the contracture completely. 5. Nifedipine and Ni2+ depressed the nerve stimulation-evoked twitch response and tetanic contracture as well as acetylcholine contracture. 6. These observations suggest that, in the myenteric plexus, a subset of N-type Ca2+ channel dominates under low frequency stimulation, while high frequency stimulation may recruit additional channels and non-cholinergic pathways.
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