Neurogenic control of myoelectric complexes in the mouse isolated colon

Lyster, D. J. K.; Bywater, Robert A.R.; Taylor, Grahame S.

doi:10.1016/0016-5085(95)90684-3

Cited by 83 publications

(137 citation statements)

References 19 publications

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“…The shape of the small and large intestine in mammals resembles an elongated hollow organ. In contrast to simple tubes, however, the gut has to generate the force needed to ensure intraluminal transport (6,14). Accordingly, a sophisticated neural and muscular network (6,8,9,17,24) has emerged in the course of evolution (2,7,10,11,17,26,27).…”

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confidence: 99%

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Structural differences in the enteric neural network in murine colon: impact on electrophysiology

Sibaev

Franck²,

Vanderwinden³

et al. 2003

American Journal of Physiology-Gastrointestinal and Liver Physi

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The enteric neural network in the proximal murine colon shows a regularly occurring hypoganglionic region, which is here characterized by using anatomical and electrophysiological techniques. Staining with NADPH diaphorase, methylene blue, and cuprolinic blue in standard whole mounts and three-dimensional gut preparations of the murine proximal colon consistently revealed two hypoganglionic areas surrounded by a dense clustering of enteric neurons. This irregularity in the ganglionic plexus was found to be present in mice of three different genetic backgrounds, as well as in rats. The lack of myenteric ganglia in these regions was associated with an absence of the longitudinal muscle layer, as shown in cross sections. Histochemical identification of interstitial cells of Cajal in Kit W-lacZ/ϩ transgenic mice showed Kit-positive cells oriented parallel to both muscle layers of the colon. Kit-positive cells oriented parallel to the longitudinal muscle layers were absent in the hypoganglionic area described. Electrical field stimulation elicited TTX-sensitive inhibitory junction potentials (IJPs), which showed region-specific characteristics. The initial partly apamin-sensitive hyperpolarization was present in all parts of the murine colon, whereas a second sustained N G -nitro-L-argininesensitive hyperpolarization was absent in the cecum and decreased from the proximal to the distal colon. Dissecting the hypoganglionic area from the surrounding tissue abolished the otherwise normal inhibitory neurotransmission to the circular muscle (1.6 Ϯ 1.4 and 2.6 Ϯ 1.7 mV for the fast and slow component of IJP amplitude in the hypoganglionic area vs. 16.5 Ϯ 1.9 and 23.7 Ϯ 2.7 mV for the fast and slow component of IJP amplitude in the neuron-rich area, respectively, P Ͻ 0.01, n ϭ 6), whereas dissection of an area of identical size with an intact myenteric network showed normal inhibitory neurotransmission, indicating that the hypoganglionic area receives essential functional neural input from the neuron-rich surrounding tissue. In summary, in the murine and rat proximal colon, a constant and distinct hypoganglionic region is described with important concomitant changes in local electrophysiology. mouse; enteric nervous system; smooth muscle; inhibitory junction potentials SINCE THE ORIGINAL DESCRIPTION of the enteric nervous system in the small bowel by Auerbach (1), it has been believed that the enteric ganglia form a regular network over the entire length of the gut wall. Distribution of subgroups of enteric neurons is known to vary along the longitudinal axis of the gut as demonstrated, for example, for nitric oxide (NO) synthase (NOS)-containing neurons (25, 26), but it is assumed that there is a homogeneous distribution of the neural network within a short gut segment. The shape of the small and large intestine in mammals resembles an elongated hollow organ. In contrast to simple tubes, however, the gut has to generate the force needed to ensure intraluminal transport (6,14). Accordingly, a sophisticated neural and muscul...

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confidence: 99%

“…Stimulation of intrinsic NO-dependent nerves induced mechanical relaxation of murine cecum longitudinal muscle (31) and murine proximal colon circular muscle (24). Intracellular electrical recordings of the circular muscle cells of murine colon have demonstrated functional neural input of inhibitory neurotransmitters such as NO (14,24).…”

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confidence: 99%

Structural differences in the enteric neural network in murine colon: impact on electrophysiology

Sibaev

Franck²,

Vanderwinden³

et al. 2003

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…Neuronal subtypes were examined by immunohistochemistry (Fig. 3 D, E) against calretinin (excitatory motor and a part of intrinsic primary afferent neurons) (Sang and Young, 1998;Qu et al, 2008), NOS (inhibitory motor neurons) (Lyster et al, 1995;Sang et al, 1997), and calbindin (intrinsic primary afferent neurons) (Qu et al, 2008). The proportion of calretinin-or calbindin-positive neurons to CFP-positive (rescued Ret-null) neurons remained unchanged in cKO/Bcl-xL colon as compared with control.…”

Section: Resultsmentioning

confidence: 99%

Neural Precursor Death Is Central to the Pathogenesis of Intestinal Aganglionosis inRetHypomorphic Mice

Uesaka¹,

Enomoto²

2010

J. Neurosci.

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The RET tyrosine kinase is required for the migration, proliferation, and survival of the enteric neural crest-derived cells (ENCCs) that form the enteric nervous system (ENS). Hypomorphic RET alleles cause intestinal aganglionosis [Hirschsprung disease (HSCR)], in which delayed migration and successive nonapoptotic ENCC death are considered to be major contributory factors. The significance of ENCC death in intestinal aganglionosis, however, has remained unclear. We show that elevated expression of Bcl-xL inhibits ENCC death in both Ret-null and hypomorphic states. However, the rescued Ret-null mice showed ENS malfunction with reduced nitric oxide synthase expression in colonic neurons, revealing the requirement of RET for neuronal differentiation. In contrast, the inhibition of cell death allows morphologically and functionally normal ENS formation in Ret hypomorphic mice. These results indicate that ENCC death is a principal cause of intestinal aganglionosis in a Ret hypomorphic state, and suggest that the inhibition of cell death is a route to the prevention of HSCR.

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“…This similarity is so strong that the colonic propagating contraction complexes are usually termed colonic MMCs, although they may actually be analogues of mass-movement contractions involved in defecation. Whereas IJPs are seen in the mouse colon, apamin does not affect colonic MMC cycling frequency or propagation speeds and has inconsistent effects on contraction amplitude [132,136,137].…”

Section: Functional Roles Of Purinergic Ijpsmentioning

confidence: 90%

“…However, recent developments allow some conclusions to be drawn. Isolated mouse intestine and colon exhibit periodic strong contraction complexes that propagate along the segment in a manner analogous to phase III contractions of interdigestive MMCs [132][133][134][135]. This similarity is so strong that the colonic propagating contraction complexes are usually termed colonic MMCs, although they may actually be analogues of mass-movement contractions involved in defecation.…”

Section: Functional Roles Of Purinergic Ijpsmentioning

confidence: 99%

Purinergic mechanisms in the control of gastrointestinal motility

Bornstein

2007

Purinergic Signalling

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For many years, ATP and adenosine have been implicated in movement regulation of the gastrointestinal tract. They act through three major receptor subtypes: adenosine or P1 receptors, P2X receptors and P2Y receptors. Each of these major receptor types can be subdivided into several different classes and is widely distributed amongst various neurons, muscle types, glia and interstitial cells that regulate intestinal functions. Several key roles for the different receptors and their endogenous ligands have been identified in physiological and pharmacological studies. For example, adenosine acting at A 1 receptors appears to inhibit intestinal motility in various pathological conditions. Similarly, ATP acting at P2Y receptors is an important component of inhibitory neuromuscular transmission, acting as a cotransmitter with nitric oxide. ATP acting at P2X and P2Y 1 receptors is important for synaptic transmission in simple descending excitatory and inhibitory reflex pathways. Some P2Y receptor subtypes prefer uridine nucleotides over purine nucleotides. Thus, roles for UTP and UDP as enteric transmitters in place of ATP cannot be excluded. ATP also appears to be important for sensory transduction, especially in chemosensitive pathways that initiate local inhibitory reflexes. Despite this evidence, data are lacking about the roles of either adenosine or ATP in more complex motility patterns such as segmentation or the interdigestive migrating motor complex. Clarification of roles for purinergic transmission in these common, but understudied, motility patterns will depend on the use of subtype-specific antagonists that in some cases have not yet been developed.

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Neurogenic control of myoelectric complexes in the mouse isolated colon

Cited by 83 publications

References 19 publications

Structural differences in the enteric neural network in murine colon: impact on electrophysiology

Structural differences in the enteric neural network in murine colon: impact on electrophysiology

Neural Precursor Death Is Central to the Pathogenesis of Intestinal Aganglionosis inRetHypomorphic Mice

Purinergic mechanisms in the control of gastrointestinal motility

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