Intrinsic nervous control of migrating myoelectric complexes

Sarna, Sushil K.; Stoddard, Ch; Belbeck, L.; McWade, D.

doi:10.1152/ajpgi.1981.241.1.g16

Cited by 67 publications

(46 citation statements)

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“…Bioproducts, Walkersville, MD, U.S.A.) were used for smooth muscle cell dispersion techniques. 3 [H]QNB (Du Pont NEN, Boston, MA, U.S.A.) was used for muscarinic receptor binding studies.…”

Section: Methodsmentioning

confidence: 99%

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Inflammation Inhibits Muscarinic Signaling in In Vivo Canine Colonic Circular Smooth Muscle Cells

Jadcherla

2002

Pediatr Res

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We investigated the effects of experimental colitis on the muscarinic signaling properties and contractile behavior of canine colonic circular smooth muscle. The hypotheses that inflammation 1) inhibits in vivo muscarinic receptor mediated contractions, and 2) alters receptor density or receptor-binding affinities were tested. Muscarine was infused close-intra-arterially in seven conscious dogs during normal and experimental colitis states. Colonic circular muscle contractions were recorded via surgically attached strain gauge transducers. Muscarine stimulated phasic contractions in a dose-dependent manner, whereas colitis was inhibited. The inhibitory concentration 50% dose of M 3 receptor inhibitor was several times lower than that of M 1 , M 2 , and M 4 inhibitors during normal and colitis. However, inflammation induced a significant leftward shift in the circular muscle inhibitory dose-response curve of M 2 inhibitor. Muscarinic receptor density and binding analyses in isolated circular muscle cells was done in normal and colitis states. Inflammation significantly decreased maximum binding from 4082 fmol/mg to 2708 fmol/mg, whereas affinity constant remained unaffected. The conclusions were that 1) spontaneous and muscarine-activated in vivo phasic contractile activity of colonic circular muscle cells is primarily mediated by M 3 receptors; 2) inflammation was associated with a shift in M 2 receptor potency, due chiefly to a decrease in receptor density; and 3) this inhibitory effect was seen in normal and inflamed states, suggesting the importance of M 2 receptor. These findings suggest that changes in muscarinic response during colitis may contribute to the abnormal motility seen with inflammatory bowel disease. ACh, the principal neurotransmitter of the enteric nervous system, is released not only as a result of parasympathetic activation, but also in response to many other gastrointestinal peptides (1). Atropine (nonselective muscarinic antagonist), when administered intravenously or close-intra-arterially (arterial) completely blocks all spontaneous smooth muscle contractions in the gut (1-3). In the gastrointestinal system, muscarinic receptors play a significant role in coordination of peristalsis and propulsion of luminal contents (4).The muscarinic receptors in the gut are localized at presynaptic, postsynaptic, and prejunctional and postjunctional sites (5). These receptors on smooth muscle cells mediate contractions by G-protein coupled mechanisms, whereas those at presynaptic and prejunctional sites modulate the release of ACh by negative feedback. The activation of muscarinic receptors at postsynaptic sites stimulates postsynaptic excitatory and inhibitory neurons to release neurotransmitters. The physiologic mechanisms by which muscarinic receptors stimulate in vivo colonic circular muscle contractions are not completely understood.

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“…Bioproducts, Walkersville, MD, U.S.A.) were used for smooth muscle cell dispersion techniques. 3 [H]QNB (Du Pont NEN, Boston, MA, U.S.A.) was used for muscarinic receptor binding studies.…”

Section: Methodsmentioning

confidence: 99%

“…Atropine (nonselective muscarinic antagonist), when administered intravenously or close-intra-arterially (arterial) completely blocks all spontaneous smooth muscle contractions in the gut (1)(2)(3). In the gastrointestinal system, muscarinic receptors play a significant role in coordination of peristalsis and propulsion of luminal contents (4).…”

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confidence: 99%

Inflammation Inhibits Muscarinic Signaling in In Vivo Canine Colonic Circular Smooth Muscle Cells

Jadcherla

2002

Pediatr Res

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“…Nevertheless, in knockout mice lacking pacemaker ICCs, rhythmic contractions are still present (Spencer et al, 2003). In addition, the sodium channel blocker tetrodotoxin (TTX) abolishes gut motility, suggesting that initiation and propagation of MMCs mainly depend on neuronal activity (D'Antona et al, 2001;Sarna et al, 1981;Spencer et al, 2003). The importance of a functional enteric nervous system is further emphasised in conditions such as Hirschsprung's disease, where the absence of neurons in the distal part of the gastrointestinal tract causes severe constipation as result of impaired motility (Gershon, 2002).…”

Section: Introductionmentioning

confidence: 99%

TTX-sensitive and TTX-insensitive control of spontaneous gut motility in the developing zebrafish (Danio rerio) larvae

Holmberg

Olsson

Hennig

2007

Journal of Experimental Biology

110

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SUMMARY Spontaneous regular gut motility in zebrafish begins around 4 days post fertilisation (d.p.f.) and is modulated by release of acetylcholine and nitric oxide. The role of intrinsic or extrinsic innervation for initiating and propagating the spontaneous contractions, however, is not well understood. By creating spatiotemporal maps, we could examine spontaneous motility patterns in zebrafish larvae in vivo at 4 and 7 d.p.f. in more detail. Tetrodotoxin (TTX) was added to elucidate the importance of nervous control. Anterograde and retrograde contraction waves originated in the same region,just posterior to the intestinal bulb. This area correlates well with the distribution of Hu (human neuronal protein C/D)-immunoreactive nerve cell bodies. Whereas numerous immunoreactive nerve cells were present in the mid and distal intestine at both 4 and 7 d.p.f., fewer cells were seen anterior to the origin of contractions. The overall frequency of contractions(1.16±0.15 cycles min–1, N=14 at 4 d.p.f.;1.05±0.09 cycles min–1, N=13 at 7 d.p.f.) and the interval between individual anterograde contraction waves (54.8±7.9 s at 4 d.p.f., N=14; 56.9±4.4 s, N=13 at 7 d.p.f.)did not differ between the two stages but the properties of the contractions were altered. The distance travelled by each wave increased from 591.0±43.8 μm at 4 d.p.f. (N=14) to 719.9±33.2 μm at 7 d.p.f. (N=13). By contrast, the velocity decreased from 4 d.p.f.(49.5±5.5 μm s–1, N=12) to 7 d.p.f.(27.8±3.6 μm s–1, N=13). At 4 d.p.f., TTX did not affect any of the parameters whereas at 7 d.p.f. anterograde frequency(control 1.07±0.12 cycles min–1, N=8; TTX 0.55±0.13 cycles min–1, N=8) and distance travelled (control 685.1±45.9 μm, N=8; TTX 318.7±88.7 μm, N=6) were decreased. In conclusion, enteric or extrinsic innervation does not seem to be necessary to initiate spontaneous contractions of the gut in zebrafish larvae. However, later in development,nerves have an increasingly important role as modulators of intestinal activity.)

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“…Small intestinal segments divided by transection and reanastomosed also generate their own MMC cycles independent of other segments [20,21]. It has been reported that bolus injection of atropine (anticholinergic antagonist), hexamethonium (ganglionic blocking agent), and tetrodotoxin (neuronal transmission blocking agent) via an intra-arterial catheter to the intestinal segment blocked phase 3 propagation at the perfused site [22]. Thus, these observations suggest that the initiation and propagation of the MMC are under intrinsic neural control, which is inherent to the enteric nervous system in the intestinal wall.…”

Section: Discussionmentioning

confidence: 99%

Intestinal Neuromuscular Function after Preservation and Transplantation

Hamada¹,

Hutson²,

Nakada³

et al. 1996

Journal of Surgical Research

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While it is well known that prolonged preservation of the intestinal graft causes severe mucosal damage after transplantation, little is known about the effect on neuromuscular function. The entire small intestine of adult hound dogs was flushed and preserved with cold lactated Ringer's solution and autotransplanted either immediately (n = 6) or after 24 hr (n = 6). Animals undergoing sham operation (n = 4) were used as a control. Fasting motility and the response of the intestinal smooth muscle and enteric nerves to bethanechol (100 μg/kg/0.5 hr, iv) and cisapride (0.5 mg/kg, iv) were determined by a multiple strain gauge method on Postoperative Days 2, 4, 7, 14, 21, and 28. Compared to the control, immediately transplanted grafts and those preserved for 24 hr developed delayed reappearance of migrating myoelectric complexes (MMC), hypercontractile activity, and reduced response to bethanechol and cisapride administration. Animals in the preservation group developed more abnormal fasting motility after transplantation, but responses to bethanechol and cisapride stimulation were not markedly different from those of the immediate group. The reappearance of MMC occurred 3 weeks postoperatively in the preservation group compared to 2 days in the immediate group. The results of our study indicate that intestinal dysmotility is augmented in prolonged-preservation grafts compared to those with brief preservation. The dysmotility was transient and normalized 3 to 4 weeks after surgery. Preservation and reperfusion injury to the neuromuscular system of intestinal grafts are reversible and are attenuated by simple hypothermia.

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Intrinsic nervous control of migrating myoelectric complexes

Cited by 67 publications

References 0 publications

Inflammation Inhibits Muscarinic Signaling in In Vivo Canine Colonic Circular Smooth Muscle Cells

Inflammation Inhibits Muscarinic Signaling in In Vivo Canine Colonic Circular Smooth Muscle Cells

TTX-sensitive and TTX-insensitive control of spontaneous gut motility in the developing zebrafish (Danio rerio) larvae

Intestinal Neuromuscular Function after Preservation and Transplantation

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