Acute Experimental Distal Colitis Alters Colonic Transit in Rats

Myers, Brian S.; Dempsey, Daniel T.; Yasar, Saban; Martin, John S.; Parkman, Henry P.; Ryan, James P.

doi:10.1006/jsre.1997.5042

Cited by 26 publications

(11 citation statements)

References 20 publications

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“…Similar projections of IMG neurons to the colon could conceivably provide a low threshold reflex pathway modulating motor patterns. Interestingly, acute colitis has marked effects on colonic transit, consistent with sympathetic activation (Myers et al, 1997a), but also potentially because of altered contractility of smooth muscle (Goldhill et al, 1995;Myers et al, 1997b). SOM neurons in the IMG project to both the myenteric and submucosal plexuses (Parr and Sharkey, 1996) and might therefore modulate all enteric nerve f unctions.…”

Section: Discussionmentioning

confidence: 93%

Immediate-Early Gene Expression in the Inferior Mesenteric Ganglion and Colonic Myenteric Plexus of the Guinea Pig

1999

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Activation of neurons in the inferior mesenteric ganglion (IMG) was assessed using c-fos, JunB, and c-Jun expression in the guinea pig IMG and colonic myenteric plexus during mechanosensory stimulation and acute colitis in normal and capsaicin-treated animals. Intracolonic saline or 2% acetic acid was administered, and mechanosensory stimulation was performed by passage of a small (0.5 cm) balloon either 4 or 24 hr later. Lower doses of capsaicin or vehicle were used to activate primary afferent fibers during balloon passage. c-Jun did not respond to any of the stimuli in the study. c-fos and JunB were absent from the IMG and myenteric plexus of untreated and saline-treated animals. Acetic acid induced acute colitis by 4 hr, which persisted for 24 hr, but c-fos was found only in enteric glia in the myenteric plexus and was absent from the IMG.Balloon passage induced c-fos and JunB in only a small subset of IMG neurons and no myenteric neurons. However, balloon passage induced c-fos and JunB in IMG neurons (notably those containing somatostatin) and the myenteric plexus of acetic acid-treated animals. After capsaicin treatment, c-fos and JunB induction by balloon passage was inhibited in the IMG, but there was enhanced c-fos expression in the myenteric plexus. c-fos and JunB induction by balloon stimulation was also mimicked by acute activation of capsaicin-sensitive nerves. These data suggest that colitis enhances reflex activity of the IMG by a mechanism that involves activation of both primary afferent fibers and the myenteric plexus.

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Section: Discussionmentioning

confidence: 93%

Immediate-Early Gene Expression in the Inferior Mesenteric Ganglion and Colonic Myenteric Plexus of the Guinea Pig

1999

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“…The activation of NK 2 receptors largely supports the enhancement of cholinergic activity during colonic irritation since nepadutant consistently reduced acetic acid‐induced colonic motility. Since, previous studies have determined that low doses of NKA enhances the intestinal transit in an atropine‐sensitive manner ( Holzer, 1985 ), acetic acid‐induced colonic motility could also be associated to an increased propulsive function ( Myers et al ., 1997 ) thus contributing to the symptoms of diarrhoea ( Croci et al ., 1997 ; Makridis et al ., 1999 ).…”

Section: Discussionmentioning

confidence: 99%

Tachykinin NK₂ receptors and enhancement of cholinergic transmission in the inflamed rat colon: an in vivo motility study

Carini¹,

Lecci²,

Tramontana³

et al. 2001

British J Pharmacology

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1 In the gastrointestinal tract, tachykinin NK 2 receptors are localized both on smooth muscle and nerve ®bres. NK 2 receptor antagonists reduce exaggerated intestinal motility in various diarrhoea models but the site of action contributing to this e ect is unknown. In this study we investigated the e ects of atropine (1.4 mmol kg 71 , i.v.), hexamethonium (13.5 mmol kg 71 , i.v.), and nepadutant (0.1 mmol kg 71 , i.v.), a selective tachykinin NK 2 receptor antagonist, on distension (0.5 and 1 ml)-, or irritation (acetic acid, 0.5 ml of 7.5% v v 71 )-induced motility in the rat distal colon in vivo. The e ects of atropine, hexamethonium or N o -nitro-L-argininemethylester (L-NAME, 1.85 mmol kg 71 , i.v.) on [bAla 8 ]NKA(4-10) (10 nmol kg 71 , i.v.)-induced colonic contractions were also investigated. 2 When the colonic balloon was ®lled with a subthreshold volume (0.5 ml), the intraluminal instillation of acetic acid triggered a high-amplitude phasic colonic motility which was partially reduced by nepadutant and suppressed by either hexamethonium or atropine. Filling of the balloon with 1 ml evoked re¯ex (hexamethonium-sensitive), atropine-sensitive phasic colonic motility: nepadutant had no signi®cant e ect on the distension-evoked motility. 3 Neither hexamethonium nor atropine signi®cantly reduced [bAla 8 ]NKA(4-10)-induced colonic contractions, whereas nepadutant suppressed them. Following L-NAME pretreatment, [bAla 8 ]N-KA(4-10)-induced colonic contractions were inhibited by both atropine and hexamethonium. In hexamethonium-pretreated animals, an atropine-sensitive component of [bAla 8 ]NKA(4-10)-induced colonic contractions was also evident. 4 These results indicate that the application of irritants onto the colonic mucosa induces the release of endogenous tachykinins which enhance excitatory cholinergic mechanisms through the stimulation of NK 2 receptors.

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“…83 In contrast, it has been shown that diarrhea is associated with rectosigmoid irritability rather than rapid transit in patients with ulcerative colitis (UC). 84 Colonic transit is delayed in patients with active distal colitis 84,85 and in rats with acetic acid-induced colitis, 86 while colonic transit is normal in patients with quiescent colitis. 87 Thus, colonic transit seems to vary with the degree of inflammation, as well as species studied.…”

Section: Large Intestinementioning

confidence: 99%

Pathophysiological significance of neuronal nitric oxide synthase in the gastrointestinal tract

Takahashi

2003

Journal of Gastroenterology

242

181

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It has been demonstrated that nitric oxide (NO) is a major inhibitory nonadrenergic, noncholinergic (NANC) neurotransmitter in the gastrointestinal (GI) tract. NO released in response to nerve stimulation of the myenteric plexus causes relaxation of the smooth muscle. NO is synthesized by the activation of neuronal NO synthase (nNOS) in the myenteric plexus. Released NO plays an important physiological role in various parts of the GI tract. NO regulates the muscle tone of the sphincter in the lower esophagus, pylorus, sphincter of Oddi, and anus. NO also regulates the accommodation reflex of the fundus and the peristaltic reflex of the intestine. Previous studies have shown that NOS inhibitors delay gastric emptying and colonic transit. The reduction of nNOS expression, associated with impaired local production of NO, may be responsible for motility disorders in the GI tract. There is accumulated evidence that dysfunction of NO neurons in the myenteric plexus may cause various GI diseases. These reports are reviewed and possible mechanisms of altered nNOS expression are discussed in this article. In particular, impaired nNOS synthesis of the myenteric plexus seems to be an important contributing factor to the pathogenesis of achalasia, diabetic gastroparesis, infantile hypertrophic pyloric stenosis, Hirschsprung's disease, and Chagas' disease. Reduced NO release and/or nNOS expression are suspicious in a subset of patients with functional dyspepsia. Although the etiology of intestinal pseudo-obstruction remains unknown, it is conceivable that extrinsic denervation may upregulate nNOS expression, resulting in enhanced muscular relaxation and disturbed peristalsis. An animal model of colitis showed impaired nNOS expression in the colonic myenteric plexus. Antecedent infection may be associated with the impaired NO pathways observed in functional dyspepsia, colitis, and Chagas' disease.

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Acute Experimental Distal Colitis Alters Colonic Transit in Rats

Cited by 26 publications

References 20 publications

Immediate-Early Gene Expression in the Inferior Mesenteric Ganglion and Colonic Myenteric Plexus of the Guinea Pig

Immediate-Early Gene Expression in the Inferior Mesenteric Ganglion and Colonic Myenteric Plexus of the Guinea Pig

Tachykinin NK₂ receptors and enhancement of cholinergic transmission in the inflamed rat colon: an in vivo motility study

Pathophysiological significance of neuronal nitric oxide synthase in the gastrointestinal tract

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Acute Experimental Distal Colitis Alters Colonic Transit in Rats

Cited by 26 publications

References 20 publications

Immediate-Early Gene Expression in the Inferior Mesenteric Ganglion and Colonic Myenteric Plexus of the Guinea Pig

Immediate-Early Gene Expression in the Inferior Mesenteric Ganglion and Colonic Myenteric Plexus of the Guinea Pig

Tachykinin NK2 receptors and enhancement of cholinergic transmission in the inflamed rat colon: an in vivo motility study

Pathophysiological significance of neuronal nitric oxide synthase in the gastrointestinal tract

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Tachykinin NK₂ receptors and enhancement of cholinergic transmission in the inflamed rat colon: an in vivo motility study