Muscarinic cholinergic receptor density following small intestinal transplantation in rats

Zhang, Zheng; Koch, Timothy R.; Mustin, E.; Walgenbach-Telford, Susan; Telford, Gordon L.

doi:10.1152/ajpgi.1993.265.6.g1057

Cited by 8 publications

(10 citation statements)

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“…Previous examination of nerve cell products did not support neuronal cell loss after transplantation [10]. We have no evidence to support a change in primary DNA structure following transplantation.…”

Section: Discussioncontrasting

confidence: 77%

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Distribution of Muscarinic Receptor Subtypes in Rat Small Intestine

Stadelmann¹,

Walgenbach-Telford²,

Telford³

et al. 1998

Journal of Surgical Research

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Section: Discussioncontrasting

confidence: 77%

“…We have determined the total muscarinic receptor density in samples from sham-operated rats, rats in which the proximal 50% of small intestine was resected, and rats with transplantation of the distal 50% of small intestine [10]. There was no evidence supporting loss of intrinsic cholinergic neurons.…”

Section: Introductionmentioning

confidence: 99%

Distribution of Muscarinic Receptor Subtypes in Rat Small Intestine

Stadelmann¹,

Walgenbach-Telford²,

Telford³

et al. 1998

Journal of Surgical Research

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“…Downregulation of muscarinic receptors may explain the shift of the cholinergic contraction to one that is NANC mediated. Such downregulation has been implicated after massive intestinal resection38 or intestinal transplantation39and a subsensitivity to acetylcholine has been noted in bypassed ileum (own unpublished results). A downregulation of muscarinic receptors may also be reflected in a failure to release neuronal NO as acetylcholine was found to release NO as studied in rat colon 40.…”

Section: Discussionmentioning

confidence: 87%

Structural, neuronal, and functional adaptive changes in atrophic rat ileum

Ekelund

Ekblad

1999

Gut

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Background-Inactivity of the gut leads to atrophic changes of which little is known. Aims-To investigate structural, neuronal, and functional changes occurring in bypassed rat ileum. Methods-Morphometry was used to characterise the atrophic changes. The numbers of enteric neurones, their expression of neurotransmitters, and the presence of interstitial cells of Cajal were studied using immunocytochemistry and in situ hybridisation. Motor activity was studied in vitro. Results-Adaptive changes in bypassed ileum include atrophy and remodelling of the gut wall. The total numbers of submucous and myenteric neurones per unit length increased one and four weeks after bypass but were identical to sham operated intestine 10 weeks after bypass. Neurones expressing vasoactive intestinal peptide, neuropeptide Y, or pituitary adenylate cyclase activating peptide decreased gradually in number in bypassed ileum. Nitric oxide synthase expressing neurones were increased, particularly in the myenteric ganglia. No change in the frequency and distribution of interstitial cells of Cajal was noted. The contractile response elicited by electrical stimulation of sham operated ileum consisted of a fast cholinergic twitch followed by a slower non-adrenergic, non-cholinergic contraction. In the bypassed ileum an identical biphasic contraction was elicited; however, the entire response was nonadrenergic, non-cholinergic. The relaxatory response to electrical stimulation in sham operated ileum was nitric oxide mediated; after bypass it was nonnitrergic. Conclusions-Notable atrophic changes were seen in the rat ileum after bypass. The enteric nervous system reacted with neuronal cell death and plasticity in terms of release and expression of neurotransmitters. (Gut 1999;45:236-245)

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“…The inhibitory effect of colonic inflammation on spontaneous phasic contractions has been observed in earlier studies (9 -11). In vitro, at the myenteric plexus level at least in rats, excitatory neuronal function may be inhibited, resulting in a decrease in the release of ACh (12), whereas at the circular muscle cell, there may be a decrease in the density or affinity of muscarinic receptors (13).…”

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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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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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Muscarinic cholinergic receptor density following small intestinal transplantation in rats

Cited by 8 publications

References 0 publications

Distribution of Muscarinic Receptor Subtypes in Rat Small Intestine

Distribution of Muscarinic Receptor Subtypes in Rat Small Intestine

Structural, neuronal, and functional adaptive changes in atrophic rat ileum

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

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