A new model of pacing in the mouse intestine

Daniel, E. E.; Boddy, Geoffrey; Bong, Alicia; Cho, Woo-Jung

doi:10.1152/ajpgi.00221.2003

Cited by 29 publications

(49 citation statements)

References 58 publications

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“…However, examination of the applicability of these data to intact intestines remains an important question. We have demonstrated that pacing in undissected segments of mouse intestines after nerve block is similar in several respects to the pacing observed in cultured or dissected mouse intestines (4). Both exhibit TTX and L-type Ca 2ϩ channel independence, high temperature dependence, jejunum faster than ileum, and in W/W V intestine, lacking ICC-MP, CM is poorly active.…”

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confidence: 53%

ICC pacing mechanisms in intact mouse intestine differ from those in cultured or dissected intestine

Boddy

Bong

Cho

et al. 2004

American Journal of Physiology-Gastrointestinal and Liver Physi

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Pacing of mouse intestine is driven by spontaneous activity of a network of interstitial cells of Cajal in the myenteric plexus (ICC-MP). So far, highly dissected circular muscle (CM) strips from control and mutant mice lacking ICC-MP and isolated, cultured ICC from newborn control mice were used to analyze its properties. Using intact circular and longitudinal segments of intestine, we recently reported that there were both significant similarities and differences between pacing studied in segments and from isolated, dissected tissues. Here, we report additional similarities and differences in our model from those in highly reduced systems. Similar to cultured or dissected intestine, blockade of sarcoplasmicendoplasmic reticulum Ca 2ϩ pumps with thapsigargin or cyclopiazonic acid reduced pacing frequency, but thapsigargin was less effective than in isolated, cultured ICC. Moreover, inhibition of inositol 1,4,5-trisphosphate (IP3) receptors with xestospongin C, a putative inhibitor of IP3 receptors, failed to affect pacing but successfully blocked increased pacing frequency by phorbol ester. 2-Aminoethoxy-diphenylborate, a putative blocker of IP 3-mediated calcium release, caused a significant decrease in the amplitude and frequency of contractions. The mitochondrial uncoupler carbonyl cyanide ptrifluormethoxyphenylhydrazone blocked pacing and KCl-induced contractions at a concentration of 1 M. The cyclic nucleotide agonists sodium nitroprusside (SNP), forskolin, and 8-bromo-cGMP inhibited pacing in CM. In longitudinal muscle (LM), SNP and forskolin had little effect on pacing. Furthermore, dibutyryl-cAMP did not affect pacing in CM or LM. These results suggest that pacing in intact intestine is under partly similar regulatory control as in more reduced systems. However, pacing in intact intestine is not affected by xestospongin C, which abolishes pacing in isolated, cultured ICC and exhibits attenuated responses to thapsigargin. Also, major differences between LM and CM suggest a separate pacemaker may drive LM.

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confidence: 53%

ICC pacing mechanisms in intact mouse intestine differ from those in cultured or dissected intestine

Boddy

Bong

Cho

et al. 2004

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…Although Daniel et al (2002) reported the presence of cyclic mechanical activity (slower in the ileum than jejunum) in the longitudinal and circular muscle of the small intestine in the W/W V mutant mouse, we have recently shown that spontaneous electrical and mechanical activities of the longitudinal and circular muscle were significantly different between the ileum and jejunum in the W/W V mutant mouse (Nakagawa et al, 2003(Nakagawa et al, , 2005. Furthermore, we found that tight synchronicity between longitudinal and circular muscle contraction was present in the segments of jejunum and ileum even in the W/W V mouse.…”

Section: Discussionmentioning

confidence: 99%

“…We have previously reported that spontaneous rhythmic contractions are observed in the proximal colon of Ws/Ws rats, where there is a deficiency of both ICC in the myenteric region (ICC-MY) and of ICC-SM (Yoneda et al, 2001). Furthermore, it has been reported that smooth muscle preparations of the small intestine (duodenum, jejunum or ileum) of W/W V mutant mice show a variety of electrical activities (Malysz et al, 1996), longitudinal cyclic contractions (Daniel et al, 2002) and distension-induced peristalsis . In the small intestine of W/W V mutant mice, while ICC-MY are absent, the ICC of the deep muscular plexus region (ICC-DMP) are present (Malysz et al, 1996;Takayama et al, 2001Takayama et al, , 2002.…”

Section: Introductionmentioning

confidence: 99%

Absence of peristalsis in the ileum of W/WV mutant mice that are selectively deficient in myenteric interstitial cells of Cajal

Nakagawa

Misawa

Nakajima

et al. 2005

J. Smooth Muscle Res.

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It is well known that the enteric nervous system plays a key role in the generation of gastrointestinal peristaltic movements. Recently, the networks of interstitial cells of Cajal (ICC) have been found to be essential in the generation of spontaneous gastrointestinal movements. However, the role of ICC in the mechanisms involved in the generation of peristaltic movements is still controversial. The aim of the present study was to reveal how pacemaker myenteric ICC (ICC-MY) and the enteric nervous system contribute to the mechanisms involved in the generation of intestinal peristalsis. We compared spontaneous peristaltic movements of the ileum in wild type (WT) mice with those in W/W V mutant mice which are selectively deficient in ICC-MY. Simultaneous recordings were made from both the circular and longitudinal muscle of a 4-cm long segment of ileum under hydrostatic pressure of 0-0.5 cm H2O. Mechanical activity and continuous videoimages of the ileum were compared between WT and W/W V mutant mice under control conditions, in the presence of N-nitro-L-arginine methyl ester (L-NAME) and after tetrodotoxin (TTX). In the WT mouse ileum, peristaltic waves to propagate from the oral to the anal end were frequently observed. The frequency of these peristaltic waves and their associated synchronous longitudinal and circular muscle contractions was increased by L-NAME. The peristaltic waves were abolished by TTX. In the W/W V mutant mouse ileum, no peristaltic waves to propagate from the oral to the anal end were observed in control and even after L-NAME, although the local spontaneously generated longitudinal and circular muscle contractions were enhanced by L-NAME. These local contractions were not abolished by TTX. The results presented here suggested that ICC-MY are essential for the generation of spontaneous intestinal peristaltic movements. It is conceivable that ICC-MY may determine the polarity of the excitation of the intestine such that longitudinal and circular muscle contractions propagate from the oral to the anal end of the intestinal segments, although the question of why ICC-MY are necessary for the neural pathways remains unresolved.

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“…39 Similar findings were also reported in in vitro studies in ICC knocked out mice. 40,41 Because of its pacing capability, GES with long pulses is also able to induce tachygastria when delivered at a tachygastrial frequency (a frequency higher than the physiological frequency). 42,43 GES-induced tachygastria was reported to be associated with antral hypomotility, mediated via the adrenergic pathway.…”

Section: Alterations Of Gastric Slow Wavesmentioning

confidence: 99%