Neural mechanisms underlying migrating motor complex formation in mouse isolated colon

Brierley, Stuart M.; Nichols, Kim; Grasby, Dallas J.; Waterman, Sally A.

doi:10.1038/sj.bjp.0703814

Cited by 66 publications

(89 citation statements)

References 38 publications

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“…Addition of the NK 2 antagonist GR159897 decreasedfecal pellet motility in3 month colons but was without effect in the 24 month group consistent with NK 2 -mediated signaling being naturally impaired in this age group. These results support those from other studies,which have also shown that NK 2 blockade can reduce the amplitude of colonic migrating motor complexes (CMMCs), a motility pattern believed to contribute to fecal pellet propulsion (Brierley et al, 2001). The precise causes ofthe decrease in NK 2 -mediated signaling are unclear and may possibly reflect the loss of myenteric neurones,whichhas been recorded in many species including humans (Saffrey, 2013).However, we have recently shown that myenteric neuronal numbers do not decrease with age in the distal colon of the C57BL/6J male mice suggesting that the changes observed reflect the altered functioning of a fixed neuronal pool (Gamage et al, 2013).…”

Section: Accepted M Manuscriptsupporting

confidence: 82%

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Impaired colonic motility and reduction in tachykinin signalling in the aged mouse

Patel

Fidalgo

et al. 2014

Experimental Gerontology

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Section: Accepted M Manuscriptsupporting

confidence: 82%

“…Tachykinins are one of theimportant regulators of colonic motility in mice (Brierley et al, 2001;Deiteren et al, 2011;Mulè et al, 2007). Tachykininsregulate colonic motility via NK 1 and NK 2 receptors.…”

Section: Accepted Manuscriptmentioning

confidence: 99%

Impaired colonic motility and reduction in tachykinin signalling in the aged mouse

Patel

Fidalgo

et al. 2014

Experimental Gerontology

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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: 93%

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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“…Colonic migrating motor complexes (CMMCs) result from a complicated interplay between enteric afferent neurons, interneurons, and motor neurons and comprise a major motor pattern involved in moving fecal matter along the bowel (24)(25)(26). In the current study, CMMCs were studied using previously described methods (20,27,28) with minor modifications. Male BALB/c, C57BL/6, and M2R-or M3R-knockout mice (ages 10-12 weeks, 20-30 gm) were killed and the colons excised and suspended in a 100-ml organ bath containing Krebs-Ringer solution with 95% O 2 /5% CO 2 (pH 7.4) at 37°C.…”

Section: Methodsmentioning

confidence: 99%

“…In this assay, spontaneous, regular CMMCs were recorded as contractions migrating from the proximal to the distal colon at intervals of 2-3 minutes, separated by periods of quiescence, during which inhibitory motor activity occurs (28,35) (Figures 1A and 4A). …”

Section: Park Et Almentioning

confidence: 99%

Antibodies interfering with the type 3 muscarinic receptor pathway inhibit gastrointestinal motility and cholinergic neurotransmission in Sjögren's syndrome

Park¹,

Haberberger²,

Gordon³

et al. 2011

Arthritis & Rheumatism

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Objective. In primary Sjögren's syndrome (SS), impairment of the gastrointestinal (GI) tract is common, and includes reduced esophageal motor function, delayed gastric emptying, and abnormalities in colonic motility; the pathogenesis is as yet unknown. We undertook this study to investigate the role of functional antibodies to the type 3 muscarinic receptor (M3R) in GI dysfunction associated with primary SS.Methods. Muscle strip and whole-organ functional assays were used to determine whether IgG with anti-M3R activity from patients with primary SS disrupted neurotransmission in tissue from throughout the mouse GI tract. Specificity of the autoantibody for the M3R was determined using knockout mice that were deficient in the expression of muscarinic receptor subtypes.Results. Functional antibodies to the M3R inhibited neuronally mediated contraction of smooth muscle from throughout the GI tract and disrupted complex contractile motility patterns in the colon. The autoantibodies were not active on tissue from mice that lacked the M3R, providing compelling evidence of the direct interaction of patient autoantibodies with the M3R.Conclusion. Our results indicate that anti-M3R autoantibodies have the potential to mediate multiple dysfunctions of the GI tract in primary SS, ranging from reduced esophageal motor activity to altered colonic motility. We hypothesize that altered GI motility forms part of a broader autonomic dysfunction mediated by pathogenic anti-M3R autoantibodies in primary SS.

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Neural mechanisms underlying migrating motor complex formation in mouse isolated colon

Cited by 66 publications

References 38 publications

Impaired colonic motility and reduction in tachykinin signalling in the aged mouse

Impaired colonic motility and reduction in tachykinin signalling in the aged mouse

Purinergic mechanisms in the control of gastrointestinal motility

Antibodies interfering with the type 3 muscarinic receptor pathway inhibit gastrointestinal motility and cholinergic neurotransmission in Sjögren's syndrome

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