Sodium current in human intestinal interstitial cells of Cajal

Strege, Peter R.; Ou, Yijun; Sha, Lei; Rich, Adam; Gibbons, Simon J.; Szurszewski, Joseph H.; Sarr, Michael G.; Farrugia, Gianrico

doi:10.1152/ajpgi.00152.2003

Cited by 132 publications

(178 citation statements)

References 38 publications

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“…The observation that families with SCN5A-related cardiac channelopathies report much higher incidence of abdominal pain than a control population has led to the hypothesis that sodium channelopathies may be a contributing cause in the pathogenesis of functional bowel disorders (67). The Na v 1.5 voltage-gated sodium channel encoded by SCN5A is expressed in human jejunal epithelial cells and interstitial cells of Cajal (68). In a study of an IBS cohort, one patient with a family history of IBS exhibited a loss-of-function G298S missense mutation on a background of a common H558R polymorphism in SCN5A (69).…”

Section: Visceral Painmentioning

confidence: 99%

Pain as a channelopathy

Raouf¹,

Quick

Wood

2010

J. Clin. Invest.

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Mendelian heritable pain disorders have provided insights into human pain mechanisms and suggested new analgesic drug targets. Interestingly, many of the heritable monogenic pain disorders have been mapped to mutations in genes encoding ion channels. Studies in transgenic mice have also implicated many ion channels in damage sensing and pain modulation. It seems likely that aberrant peripheral or central ion channel activity underlies or initiates many pathological pain conditions. Understanding the mechanistic basis of ion channel malfunction in terms of trafficking, localization, biophysics, and consequences for neurotransmission is a potential route to new pain therapies.

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Section: Visceral Painmentioning

confidence: 99%

Pain as a channelopathy

Raouf¹,

Quick

Wood

2010

J. Clin. Invest.

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“…Strege et al [24] suggested that a mechanosensitive Na + channel current is present in human intestinal ICC and appears to play a role in the control of intestinal motor function. Also in human jejunum, each ICC-MY generates spontaneous pacemaker activity that actively propagates through the ICC network, and the pacemaker activity was dependent on inositol-1,4,5-triphosphate receptor-operated stores and mitochondrial function [25] .…”

Section: Kim Bj Et Al Trpm7 and Interstitial Cells Of Cajalmentioning

confidence: 99%

Identifcation of TRPM7 channels in human intestinalinterstitial cells of Cajal

Kim¹,

Park²,

Kim³

et al. 2009

WJG

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AIM:To investigate the characteristics of slow electrical waves and the presence of transient receptor potential melastatin-type 7 (TRPM7) in the human gastrointestinal (GI) tract. METHODS:Conventional microelectrode techniques were used to record intracellular electrical responses from human GI smooth muscle tissue. Immunohistochemistry was used to identify TRPM7 channels in interstitial cells of Cajal (ICCs). RESULTS:The human GI tract generated slow electrical waves and had ICCs which functioned as pacemaker cells. Flufenamic acid, a nonselective cation channel blocker, and 2-APB (2-aminoethoxydiphenyl borate) and La 3+, TRPM7 channel blockers, inhibited the slow waves. Also, TRPM7 channels were expressed in ICCs in human tissue. CONCLUSION:These results suggest that the human GI tract generates slow waves and that TRPM7 channels expressed in the ICCs may be involved in the generation of the slow waves.

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“…33,34 Therefore, ICC determine the frequency of contractions. Additionally, ICC act as amplifiers of neuronal signals, 35,36 as mechanosensors, 37 and to set the smooth muscle membrane potential gradient. 38 A decreased number of ICC or a disrupted ICC network is associated with pathologic conditions such as slow transit constipation, 39,40 diabetic gastroparesis, 41 and pseudo-obstruction.…”

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confidence: 99%