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Calcium-associated mechanisms in gut pacemaker activity.

Nakayama S, Kajioka S, Goto K, Takaki M, Liu HN - J. Cell. Mol. Med. (2007 Sep-Oct)

Bottom Line: A considerable body of evidence has revealed that interstitial cells of Cajal (ICC), identified with c-Kit-immunoreactivity, act as gut pacemaker cells, with spontaneous Ca(2+) activity in ICC as the probable primary mechanism.Namely, intracellular (cytosolic) Ca(2+) oscillations in ICC periodically activate plasmalemmal Ca(2+)-dependent ion channels and thereby generate pacemaker potentials.This review will, thus, focus on Ca(2+)-associated mechanisms in ICC in the gastrointestinal (GI) tract, including auxiliary organs.

View Article: PubMed Central - PubMed

Affiliation: Department of Cell Physiology, Nagoya University Graduate School of Medicine, Nagoya, Japan. h44673a@nucc.cc.nagoya-u.ac.jp

ABSTRACT
A considerable body of evidence has revealed that interstitial cells of Cajal (ICC), identified with c-Kit-immunoreactivity, act as gut pacemaker cells, with spontaneous Ca(2+) activity in ICC as the probable primary mechanism. Namely, intracellular (cytosolic) Ca(2+) oscillations in ICC periodically activate plasmalemmal Ca(2+)-dependent ion channels and thereby generate pacemaker potentials. This review will, thus, focus on Ca(2+)-associated mechanisms in ICC in the gastrointestinal (GI) tract, including auxiliary organs.

Show MeSH
The action sites of drugs on Ca2+-associated mechanisms in ICC pacemaker activity. ICC and SM in this figure represent interstitial cells of Cajal and smooth muscle cells, respectively. For other abbreviations, see text.
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fig01: The action sites of drugs on Ca2+-associated mechanisms in ICC pacemaker activity. ICC and SM in this figure represent interstitial cells of Cajal and smooth muscle cells, respectively. For other abbreviations, see text.

Mentions: Guinea-pig stomach smooth muscle, frequently used to investigate mechanisms underlying spontaneous electrical activity, referred to as slow waves [5], provides a good example with which we can assess the role of VGCC in smooth muscle tissues showing spontaneous phasic contractions. DHP Ca2+ antagonists completely abolish spontaneous contractile activity, with little effect, however, on pacemaker potentials (and electrical activity recorded from smooth muscle cells, that is, slow waves) [6, 7]. Similar spontaneous electrical activities resistant to the DHP-Ca2+ antagonist have been reported in several other GI smooth muscle tissues [8,9]. It is thus considered that DHP-sensitive L-type Ca2+ channels play an essential role in E–C coupling in GI smooth muscle cells, although these channels are not involved in the generation of pacemaker electrical activity in ICC (Fig. 1). For this reason, DHP-Ca2+ antagonists are frequently used to differentiate pacemaker electrical activity by suppressing smooth muscle activity. However, pacemaker cells in some tissues, for example, sub-mucosal ICC (ICC-SM) in the colon, produce different responses to DHP Ca2+ antagonists: 1 μM nifedipine completely abolishes the spontaneous plateau potentials [10]. Furthermore, in the guinea-pig stomach, a small inhibitory effect was observed when nifedipine was greater than 10 μM [7].


Calcium-associated mechanisms in gut pacemaker activity.

Nakayama S, Kajioka S, Goto K, Takaki M, Liu HN - J. Cell. Mol. Med. (2007 Sep-Oct)

The action sites of drugs on Ca2+-associated mechanisms in ICC pacemaker activity. ICC and SM in this figure represent interstitial cells of Cajal and smooth muscle cells, respectively. For other abbreviations, see text.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4401267&req=5

fig01: The action sites of drugs on Ca2+-associated mechanisms in ICC pacemaker activity. ICC and SM in this figure represent interstitial cells of Cajal and smooth muscle cells, respectively. For other abbreviations, see text.
Mentions: Guinea-pig stomach smooth muscle, frequently used to investigate mechanisms underlying spontaneous electrical activity, referred to as slow waves [5], provides a good example with which we can assess the role of VGCC in smooth muscle tissues showing spontaneous phasic contractions. DHP Ca2+ antagonists completely abolish spontaneous contractile activity, with little effect, however, on pacemaker potentials (and electrical activity recorded from smooth muscle cells, that is, slow waves) [6, 7]. Similar spontaneous electrical activities resistant to the DHP-Ca2+ antagonist have been reported in several other GI smooth muscle tissues [8,9]. It is thus considered that DHP-sensitive L-type Ca2+ channels play an essential role in E–C coupling in GI smooth muscle cells, although these channels are not involved in the generation of pacemaker electrical activity in ICC (Fig. 1). For this reason, DHP-Ca2+ antagonists are frequently used to differentiate pacemaker electrical activity by suppressing smooth muscle activity. However, pacemaker cells in some tissues, for example, sub-mucosal ICC (ICC-SM) in the colon, produce different responses to DHP Ca2+ antagonists: 1 μM nifedipine completely abolishes the spontaneous plateau potentials [10]. Furthermore, in the guinea-pig stomach, a small inhibitory effect was observed when nifedipine was greater than 10 μM [7].

Bottom Line: A considerable body of evidence has revealed that interstitial cells of Cajal (ICC), identified with c-Kit-immunoreactivity, act as gut pacemaker cells, with spontaneous Ca(2+) activity in ICC as the probable primary mechanism.Namely, intracellular (cytosolic) Ca(2+) oscillations in ICC periodically activate plasmalemmal Ca(2+)-dependent ion channels and thereby generate pacemaker potentials.This review will, thus, focus on Ca(2+)-associated mechanisms in ICC in the gastrointestinal (GI) tract, including auxiliary organs.

View Article: PubMed Central - PubMed

Affiliation: Department of Cell Physiology, Nagoya University Graduate School of Medicine, Nagoya, Japan. h44673a@nucc.cc.nagoya-u.ac.jp

ABSTRACT
A considerable body of evidence has revealed that interstitial cells of Cajal (ICC), identified with c-Kit-immunoreactivity, act as gut pacemaker cells, with spontaneous Ca(2+) activity in ICC as the probable primary mechanism. Namely, intracellular (cytosolic) Ca(2+) oscillations in ICC periodically activate plasmalemmal Ca(2+)-dependent ion channels and thereby generate pacemaker potentials. This review will, thus, focus on Ca(2+)-associated mechanisms in ICC in the gastrointestinal (GI) tract, including auxiliary organs.

Show MeSH