scholarly journals Ano1, a Ca2+-activated Cl−channel, coordinates contractility in mouse intestine by Ca2+transient coordination between interstitial cells of Cajal

2014 ◽  
Vol 592 (18) ◽  
pp. 4051-4068 ◽  
Author(s):  
Raman Deep Singh ◽  
Simon J. Gibbons ◽  
Siva Arumugam Saravanaperumal ◽  
Peng Du ◽  
Grant W. Hennig ◽  
...  
2004 ◽  
Vol 123 (3) ◽  
pp. 170-178 ◽  
Author(s):  
Akikazu FUJITA ◽  
Yutaka OKISHIO ◽  
Tadayoshi TAKEUCHI ◽  
Fumiaki HATA

2007 ◽  
Vol 292 (3) ◽  
pp. G734-G745 ◽  
Author(s):  
E. E. Daniel ◽  
Ahmed El Yazbi ◽  
Marco Mannarino ◽  
Gary Galante ◽  
Geoffrey Boddy ◽  
...  

Varicosities of nitrergic and other nerves end on deep muscular plexus interstitial cells of Cajal or on CD34-positive, c- kit-negative fibroblast-like cells. Both cell types connect to outer circular muscle by gap junctions, which may transmit nerve messages to muscle. We tested the hypotheses that gap junctions transmit pacing messages from interstitial cells of Cajal of the myenteric plexus. Effects of inhibitors of gap junction conductance were studied on paced contractions and nerve transmissions in small segments of circular muscle of mouse intestine. Using electrical field stimulation parameters (50 V/cm, 5 pps, and 0.5 ms) which evoke near maximal responses to nitrergic, cholinergic, and apamin-sensitive nerve stimulation, we isolated inhibitory responses to nitrergic nerves, inhibitory responses to apamin-sensitive nerves and excitatory responses to cholinergic nerves. 18β-Glycyrrhetinic acid (10, 30, and 100 μM), octanol (0.1, 0.3, and 1 mM) and gap peptides (300 μM of40Gap27,43Gap26,37,43Gap27) all failed to abolish neurotransmission. 18β-Glycyrrhetinic acid inhibited frequencies of paced contractions, likely owing to inhibition of l-type Ca2+channels in smooth muscle, but octanol or gap peptides did not. 18β-Glycyrrhetinic acid and octanol, but not gap peptides, reduced the amplitudes of spontaneous and nerve-induced contractions. These reductions paralleled reductions in contractions to exogenous carbachol. Additional experiments with gap peptides in both longitudinal and circular muscle segments after NG-nitro-l-arginine and TTX revealed no effects on pacing frequencies. We conclude that gap junction coupling may not be necessary for pacing or nerve transmission to the circular muscle of the mouse intestine.


2011 ◽  
Vol 26 (6) ◽  
pp. 1072-1078 ◽  
Author(s):  
Yimin Li ◽  
Hideto Kojima ◽  
Kazunori Fujino ◽  
Kazuhiro Matsumura ◽  
Miwako Katagi ◽  
...  

2018 ◽  
Vol 51 (6) ◽  
pp. 2887-2899 ◽  
Author(s):  
Seok Choi ◽  
Hyun Goo Kang ◽  
Mei Jin Wu ◽  
Han Yi Jiao ◽  
Dong Hoon Shin ◽  
...  

Background/Aims: Anoctamin1 (Ca2+-activated Cl- channel, ANO1) is a specific marker of the interstitial cells of Cajal (ICC) in the gastrointestinal tract, and are candidate proteins that can function as pacemaker channels. Recently, novel selective ANO1 inhibitors were discovered and used to study Ca2+-activated Cl- channels. Therefore, to investigate whether ANO1 channels function as pacemaker channels, selective ANO1 inhibitors were tested with respect to the pacemaker potentials in ICC. Methods: Whole-cell patch-clamp recording, RT-PCR, and intracellular Ca2+ ([Ca2+]i) imaging were performed in cultured ICC obtained from mice. Results: Though CaCCinh-A01 (5 µM), T16Ainh-A01 (5 µM), and MONNA (5 µM) (selective ANO1 inhibitors) blocked the generation of pacemaker potentials in colonic ICC, they did not do so in small intestinal ICC. Though nifulmic acid (10 µM) and DIDS (10 µM) (classical Ca2+-activated Cl- channel inhibitors) also had no effect in small intestinal ICC, they suppressed the generation of pacemaker potentials in colonic ICC. In addition, knockdown of ANO1 reduced the pacemaker potential frequency in colonic ICC alone. Though ANO1 inhibitors suppressed [Ca2+]i oscillations in colonic ICC, they did not do so in small intestinal ICC. T-type Ca2+ channels were expressed in the both the small intestinal and colonic ICC, but mibefradil (5 µM) and NiCl2 (30 µM) (T-type Ca2+ channel inhibitors) inhibited the generation of pacemaker potentials in colonic ICC alone. Conclusion: These results indicate that though ANO1 and T-type Ca2+ channels participate in generating pacemaker potentials in colonic ICC, they do not do so in small intestinal ICC. Therefore, the mechanisms underlying pacemaking in ICC might be different in the small intestine and the colon.


1996 ◽  
Vol 180 (1) ◽  
pp. 97-107 ◽  
Author(s):  
H.M. Young ◽  
D. Ciampoli ◽  
B.R. Southwell ◽  
D.F. Newgreen

2001 ◽  
Vol 120 (5) ◽  
pp. A201-A201 ◽  
Author(s):  
P STREGE ◽  
A RICH ◽  
Y OU ◽  
S GIBBONS ◽  
M SARR ◽  
...  

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