ArticleNeurogastroenterology and motility2016
Expression and function of the Scn5a-encoded voltage-gated sodium channel NaV 1.5 in the rat jejunum.
Article in Neurogastroenterology and motility, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- TMEM16A in smooth muscle cells acts as a pacemaker channel in the internal anal sphincter.Communications biology · 2024Article
- Review
- Tracking Gut Motility in Organ and Cultures.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Capsaicin as an amphipathic modulator of NaChannels (Austin, Tex.) · 2022Article
- Phospho-ablation of cardiac sodium channel NaInternational journal of obesity (2005) · 2021Article
- Article
- A Method for Multi-day Tracking of Gastrointestinal Smooth Muscle Contractile Patterns in Organotypic Culture.Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Annual International Conference · 2019Article
- Irritable bowel syndrome patients have SCN5A channelopathies that lead to decreased NaAmerican journal of physiology. Gastrointestinal and liver physiology · 2018Article
- Voltage-gated sodium channels: (NaThe Journal of physiology · 2018Review
- Ion channelopathies in functional GI disorders.American journal of physiology. Gastrointestinal and liver physiology · 2016Review
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Authors and funding
13 authors.
Funding
Abstract
backgroundThe SCN5A-encoded voltage-gated sodium channel NaV 1.5 is expressed in human jejunum and colon. Mutations in NaV 1.5 are associated with gastrointestinal motility disorders. The rat gastrointestinal tract expresses voltage-gated sodium channels, but their molecular identity and role in rat gastrointestinal electrophysiology are unknown.
methodsThe presence and distribution of Scn5a-encoded NaV 1.5 was examined by PCR, Western blotting and immunohistochemistry in rat jejunum. Freshly dissociated smooth muscle cells were examined by whole cell electrophysiology. Zinc finger nuclease was used to target Scn5a in rats. Lentiviral-mediated transduction with shRNA was used to target Scn5a in rat jejunum smooth muscle organotypic cultures. Organotypic cultures were examined by sharp electrode electrophysiology and RT-PCR. KEY
resultsWe found NaV 1.5 in rat jejunum and colon smooth muscle by Western blot. Immunohistochemistry using two other antibodies of different portions of NaV 1.5 revealed the presence of the ion channel in rat jejunum. Whole cell voltage-clamp in dissociated smooth muscle cells from rat jejunum showed fast activating and inactivating voltage-dependent inward current that was eliminated by Na(+) replacement by NMDG(+) . Constitutive rat Scn5a knockout resulted in death in utero. NaV 1.5 shRNA delivered by lentivirus into rat jejunum smooth muscle organotypic culture resulted in 57% loss of Scn5a mRNA and several significant changes in slow waves, namely 40% decrease in peak amplitude, 30% decrease in half-width, and 7 mV hyperpolarization of the membrane potential at peak amplitude. CONCLUSIONS & INFERENCES: Scn5a-encoded NaV 1.5 is expressed in rat gastrointestinal smooth muscle and it contributes to smooth muscle electrophysiology.
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