Tonic inhibition of murine proximal colon is due to nitrergic suppression of Ca2+ signaling in interstitial cells of Cajal

Loading...
Thumbnail Image

Authors

Drumm, Bernard T.
Rembetski, Benjamin E.
Baker, Salah A.
Sanders, Kenton M.

Issue Date

2019

Type

Article

Language

Keywords

Research Projects

Organizational Units

Journal Issue

Alternative Title

Abstract

Spontaneous excitability and contractions of colonic smooth muscle cells (SMCs) are normally suppressed by inputs from inhibitory motor neurons, a behavior known as tonic inhibition. The post-junctional cell(s) mediating tonic inhibition have not been elucidated. We investigated the post-junctional cells mediating tonic inhibition in the proximal colon and whether tonic inhibition results from suppression of the activity of Ano1 channels, which are expressed exclusively in interstitial cells of Cajal (ICC). We found that tetrodotoxin (TTX), an inhibitor of nitric oxide (NO) synthesis, L-NNA, and an inhibitor of soluble guanylyl cyclase, ODQ, greatly enhanced colonic contractions. Ano1 antagonists, benzbromarone and Ani9 inhibited the effects of TTX, L-NNA and ODQ. Ano1 channels are activated by Ca2+ release from the endoplasmic reticulum (ER) in ICC, and blocking Ca2+ release with a SERCA inhibitor (thapsigargin) or a store-operated Ca(2+ )entry blocker (GSK 7975 A) reversed the effects of TTX, L-NNA and ODQ. Ca2+ imaging revealed that TTX, L-NNA and ODQ increased Ca2+ transient firing in colonic ICC. Our results suggest that tonic inhibition in the proximal colon occurs through suppression of Ca2+ release events in ICC. Suppression of Ca2+ release in ICC limits the open probability of Ano1 channels, reducing the excitability of electrically-coupled SMCs.

Description

Citation

Drumm, B. T., Rembetski, B. E., Baker, S. A., & Sanders, K. M. (2019). Tonic inhibition of murine proximal colon is due to nitrergic suppression of Ca2+ signaling in interstitial cells of Cajal. Scientific Reports, 9(1). doi:10.1038/s41598-019-39729-7

Publisher

License

Creative Commons Attribution 4.0 International

Journal

Volume

Issue

PubMed ID

ISSN

2045-2322

EISSN

Collections