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. 2020 Jun 25;10:10378. doi: 10.1038/s41598-020-67142-y

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Proposed mechanism for the generation of pacemaker activity by Type II intramuscular interstitial cells of Cajal (Type II ICC-IM). In Type II ICC-IM, Ca²⁺ release from the endoplasmic reticulum activates the Ca²⁺-activated Cl⁻ channel ANO1 causing Cl⁻ efflux and membrane depolarisation. This in turn activates L-type voltage-dependent Ca²⁺ channels (Cav_L) on ICC-IM resulting in Ca²⁺ influx and further activation of ANO1 which in turn leads to slow wave (SW) generation (observed as a rhythmic, global Ca²⁺ transient). Depolarisation is conducted to adjacent smooth muscle cells (SMCs) via gap junctions leading to Ca²⁺ influx in SMCs via Cav_L and thus, contraction. SWs, rhythmic, global Ca²⁺ transients and tone are all abolished by the ANO1 blocker CaCCinh-A01 (10 µM) and the Cav_L blocker nifedipine (1 µM) indicating that Type II ICC-IM represent a viable candidate for generating pacemaker activity in the IAS and that these cells may therefore play an important role in tone generation. This cartoon was drawn using CorelDraw 2019 Software.