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Sci Rep. 2017 Nov 15;7(1):15650. doi: 10.1038/s41598-017-15834-3.

Sodium channel NaV1.3 is important for enterochromaffin cell excitability and serotonin release.

Author information

1
Enteric Neuroscience Program, Division of Gastroenterology & Hepatology, Department of Physiology & Biomedical Engineering, Mayo Clinic, Rochester, Minnesota, United States.
2
Division of Gastroenterology, Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts, United States.
3
Department of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, 300 Yanchang Middle Road, Shanghai, 200072, P.R. China.
4
Division of Biological Sciences, University of Missouri, Columbia, Missouri, United States.
5
Enteric Neuroscience Program, Division of Gastroenterology & Hepatology, Department of Physiology & Biomedical Engineering, Mayo Clinic, Rochester, Minnesota, United States. beyder.arthur@mayo.edu.

Abstract

In the gastrointestinal (GI) epithelium, enterochromaffin (EC) cells are enteroendocrine cells responsible for producing >90% of the body's serotonin (5-hydroxytryptamine, 5-HT). However, the molecular mechanisms of EC cell function are poorly understood. Here, we found that EC cells in mouse primary cultures fired spontaneous bursts of action potentials. We examined the repertoire of voltage-gated sodium channels (NaV) in fluorescence-sorted mouse EC cells and found that Scn3a was highly expressed. Scn3a-encoded NaV1.3 was specifically and densely expressed at the basal side of both human and mouse EC cells. Using electrophysiology, we found that EC cells expressed robust NaV1.3 currents, as determined by their biophysical and pharmacologic properties. NaV1.3 was not only critical for generating action potentials in EC cells, but it was also important for regulating 5-HT release by these cells. Therefore, EC cells use Scn3a-encoded voltage-gated sodium channel NaV1.3 for electrical excitability and 5-HT release. NaV1.3-dependent electrical excitability and its contribution to 5-HT release is a novel mechanism of EC cell function.

PMID:
29142310
PMCID:
PMC5688111
DOI:
10.1038/s41598-017-15834-3
[Indexed for MEDLINE]
Free PMC Article

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