Impaired acetylcholine release from the myenteric plexus of Trichinella-infected rats

Collins, Stephen M.; Blennerhassett, Patricia; Blennerhassett, Michael G.; Vermillion, D. L.

doi:10.1152/ajpgi.1989.257.6.g898

Cited by 65 publications

(79 citation statements)

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“…Furthermore, there were increased numbers of ChAT IR inflammatory cells in the mucosa and submucosa, many appearing to be eosinophils, which are found in significant numbers in the jejuna of nematode-infected rats (Nawa and Hirashima 1984). In light of these inflammatory changes, it is interesting that altered cholinergic metabolism in animal models of intestinal inflammation has been reported (Collins et al 1989). Because ChAT can catalyze both the degradation and synthesis of acetylcholine (Molenaar 1990), our data suggest that information obtained from tissue homogenates should be interpreted with caution.…”

Section: Figurementioning

confidence: 84%

“…However, recent studies employing immunohistochemical methods have shown alterations in tissue levels or nerve staining patterns for specific neuropeptides in gastrointestinal disorders, such as in-flammatory bowel diseases (Sjolund et al 1983;Goldin et al 1989;Strobach et al 1990;Kubota et al 1992). Furthermore, studies in experimental animals suggest that neurotransmitter metabolism might be affected by the inflammatory process (Collins et al 1989Swain et al 1991Swain et al ,1992. It has even been suggested that cholinergic nerves may participate in the interrelationship between the autonomic nervous system and the immune system (Rinner and Schauenstein 1993).…”

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confidence: 99%

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Choline Acetyltransferase (ChAT) Immunoreactivity in Paraffin Sections of Normal and Diseased Intestines

Ratcliffe

Desa

Dixon

et al. 1998

J Histochem Cytochem.

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SUMMARYThere is increasing interest in localizing nerves in the intestine, especially specific populations of nerves. At present, the usual histochemical marker for cholinergic nerves in tissue sections is acetylcholinesterase activity. However, such techniques are applicable only to frozen sections and have uncertain specificity. Choline acetyltransferase (ChAT) is also present in cholinergic nerves, and we therefore aimed to establish a paraffin section immunocytochemical technique using an anti-ChAT antibody. Monoclonal anti-choline acetyltransferase (1.B3.9B3) and a biotin-streptavidin detection system were used to study the distribution of ChAT immunoreactivity (ChAT IR) in paraffin-embedded normal and diseased gastrointestinal tracts from both rats and humans. Optimal staining was seen after 6-24 hr of fixation in neutral buffered formalin and overnight incubation in 1 g/ml of 1.B3.9B3, with a similar distribution to that seen in frozen sections. In the rat diaphragm (used as a positive control), axons and motor endplates were ChAT IR. Proportions of ganglion cells and nerve fibers in the intramural plexi of both human and rat gastrointestinal tracts were also ChAT IR, as well as extrinsic nerve bundles in aganglionic segments of Hirschsprung's disease. Mucosal cholinergic nerves, however, were not visualized. In addition, non-neuronal cells such as endothelium, epithelium, and inflammatory cells were ChAT IR. We were able to localize ChAT to nerves in formalin-fixed, paraffin-embedded sections. The presence of ChAT IR in non-neuronal cells indicates that this method should be used in conjunction with other antibodies. Nevertheless, it proves to be a useful technique for studying cholinergic neuronal distinction in normal tissues and pathological disorders.

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Section: Figurementioning

confidence: 84%

mentioning

confidence: 99%

Choline Acetyltransferase (ChAT) Immunoreactivity in Paraffin Sections of Normal and Diseased Intestines

Ratcliffe

Desa

Dixon

et al. 1998

J Histochem Cytochem.

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“…In addition, the decrease in muscarinic response may contribute to the suppression of phasic contractions during colitis. It is possible that during colitis ACh release by myenteric plexus may be decreased as noted in ileitis (12), however exogenous arterial muscarine infusion did not stimulate increased activity during colitis. Thus, these findings suggest the myogenic response is dependent on the muscarinic receptor and postreceptor activation during normal and colitis states.…”

Section: Colitis Inhibits Colonic Circular Musclementioning

confidence: 88%

“…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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“…Although lines of evidence have indicated that activation of enteric neurons is an important component of an intricate defence process aimed at eliminating T. spiralis larvae from the GI tract lumen (Collins et al, 1989;Palmer et al, 1998), the neurochemical mechanisms underlying this action remain to be clarified. It has been discovered that during the first six days of T. spiralis infection cholinergic innervation of the rat jejunum undergoes rapid alterations (Collins et al, 1989;Davis et al, 1998) whereas the levels of noradrenaline released by extrinsic nerves projecting to the jejunum fall (Swain et al, 1991). Moreover, in rats intrarectally infected with T. spiralis larvae (animal model of ulcerative colitis) several changes in neurochemical properties of enteric neurons were observed at 6 and 14 days post infection (PI; Auli et al, 2008).…”

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confidence: 99%

Expression of vasoactive intestinal polypeptide, substance P and neuropeptide Y in jejunal enteric nerves is altered in rabbits suffering from long term Trichinella spiralis infection: an immunohistochemical study

Arciszewski¹,

Nowakowski²,

Wąsowicz³

et al. 2009

Vet. Med. - Czech

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ABSTRACT:In the early intestinal stage of infection with the nematode Trichinella spiralis alterations in gut motility and chemical code of enteric neurons are observed. The present study was designed to characterize the changes in expression pattern of vasoactive intestinal polypeptide (VIP), substance P (SP) and neuropeptide Y (NPY) in enteric nerves of the rabbit jejunum occurring during long-lasting trichinellosis (35 and 42 days). Sections of the jejunum from healthy and T. spiralis-infected rabbits were processed for double immunocytochemistry in which antibodies against protein gene product 9.5 were used as a pan-neuronal marker and mixed with antisera raised against VIP, SP or NPY. At 35 and 42 days post infection a marked decrease of VIP-, SP-and NPY-immunoreactive (IR) jejunal myenteric neurons was found, whereas the expression of these neuropeptides in submucous neurons was unchanged. In the myenteric plexus and the jejunal circular muscle of T. spiralis-infected rabbits a significant reduction of VIP-IR (but not SP-IR) nerve fibres was noted. In the longitudinal muscle of the jejunum from animals with long-lasting trichinellosis the density of SP-IR nerve terminals was decreased, whereas the number of VIP-containing nerve fibres was unchanged. Long-lasting trichinellosis had no influence on NPY-IR nerve fibres in both circular and longitudinal smooth muscles. The number of NPY-positive (but not VIP-and SP-IR) nerve fibres supplying mucosa and blood vessels was decreased in T. spiralis-infected animals. These data indicate that during long-lasting trichinellosis expression of neuropeptides in jejunal enteric neurons is changed. A possible involvement of VIP and SP in persistent intestinal dysmotility and NPY in altered fluid secretion is discussed.

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Impaired acetylcholine release from the myenteric plexus of Trichinella-infected rats

Cited by 65 publications

References 0 publications

Choline Acetyltransferase (ChAT) Immunoreactivity in Paraffin Sections of Normal and Diseased Intestines

Choline Acetyltransferase (ChAT) Immunoreactivity in Paraffin Sections of Normal and Diseased Intestines

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

Expression of vasoactive intestinal polypeptide, substance P and neuropeptide Y in jejunal enteric nerves is altered in rabbits suffering from long term Trichinella spiralis infection: an immunohistochemical study

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