Su2065 LONGITUDINAL CLOSURE FOLLOWING LONGITUDINAL ENTEROTOMY CAUSES INTESTINAL STASIS AT SUTURING SITE BY IMPAIRED COLONIC MOTOR FUNCTION

Serotonin [5-hydroxytryptamine (5-HT)] acts as a modulator of colonic motility and secretion. We characterized the action of the 5-HT precursor 5-hydroxytryptophan (5-HTP) on colonic myenteric neurons and propulsive motor activity in conscious mice. Fos immunoreactivity (IR), used as a marker of neuronal activation, was monitored in longitudinal muscle/myenteric plexus whole mount preparations of the distal colon 90 min after an intraperitoneal injection of 5-HTP. Double staining of Fos IR with peripheral choline acetyltransferase (pChAT) IR or NADPH-diaphorase activity was performed. The injection of 5-HTP (0.5, 1, 5, or 10 mg/kg ip) increased fecal pellet output and fluid content in a dose-related manner, with a peak response observed within the first 15 min postinjection. 5-HTP (0.5–10 mg/kg) dose dependently increased Fos expression in myenteric neurons, with a maximal response of 9.9 ± 1.0 cells/ganglion [ P < 0.05 vs. vehicle-treated mice (2.3 ± 0.6 cells/ganglion)]. There was a positive correlation between Fos expression and fecal output. Of Fos-positive ganglionic cells, 40 ± 4% were also pChAT positive and 21 ± 5% were NADPH-diaphorase positive in response to 5-HTP, respectively. 5-HTP-induced defecation and Fos expression were completely prevented by pretreatment with the selective 5-HT4 antagonist RS-39604. These results show that 5-HTP injected peripherally increases Fos expression in different populations of cholinergic and nitrergic myenteric neurons in the distal colon and stimulates propulsive colonic motor function through 5-HT4 receptors in conscious mice. These findings suggest an important role of activation of colonic myenteric neurons in the 5-HT4 receptor-mediated colonic propulsive motor response.

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Measurement of Colonic Motor Function

Clinical Measurement in Coloproctology ◽

10.1007/978-1-4471-1822-0_2 ◽

1991 ◽

pp. 19-36 ◽

Cited By ~ 1

Author(s):

C. J. Steadman ◽

S. F. Phillips

Keyword(s):

Motor Function ◽

Colonic Motor

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Urocortin I is present in the enteric nervous system and exerts an excitatory effect via cholinergic and serotonergic pathways in the rat colon

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00066.2007 ◽

2007 ◽

Vol 293 (4) ◽

pp. G903-G910 ◽

Cited By ~ 25

Author(s):

Takazumi Kimura ◽

Tomofumi Amano ◽

Hirotsugu Uehara ◽

Hajime Ariga ◽

Tsuyoshi Ishida ◽

...

Keyword(s):

Nervous System ◽

Enteric Nervous System ◽

Motor Function ◽

Myenteric Plexus ◽

Neuronal Cells ◽

Colonic Transit ◽

Rat Colon ◽

Excitatory Effect ◽

Potent Effect ◽

Colonic Motor

Corticotropin-releasing factor (CRF) and urocortin I (UcnI) have been shown to accelerate colonic transit after central nervous system (CNS) or peripheral administration, but the mechanism of their peripheral effect on colonic motor function has not been fully investigated. Furthermore, the localization of UcnI in the enteric nervous system (ENS) of the colon is unknown. We investigated the effect of CRF and UcnI on colonic motor function and examined the localization of CRF, UcnI, CRF receptors, choline acetyltransferase (ChAT), and 5-HT. Isometric tension of rat colonic muscle strips was measured. The effect of CRF, UcnI on phasic contractions, and electrical field stimulation (EFS)-induced off-contractions were examined. The effects of UcnI on both types of contraction were also studied in the presence of antalarmin, astressin2-B, tetrodotoxin (TTX), atropine, and 5-HT antagonists. The localizations of CRF, UcnI, CRF receptors, ChAT, and 5-HT in the colon were investigated by immunohistochemistry. CRF and UcnI increased both contractions dose dependently. UcnI exerted a more potent effect than CRF. Antalarmin, TTX, atropine, and 5-HT antagonists abolished the contractile effects of UcnI. CRF and UcnI were observed in the neuronal cells of the myenteric plexus. UcnI and ChAT, as well as UcnI and 5-HT, were colocalized in some of the neuronal cells of the myenteric plexus. This study demonstrated that CRF and UcnI act on the ENS and increase colonic contractility by enhancing cholinergic and serotonergic neurotransmission. These peptides are present in myenteric neurons. CRF and, perhaps, to a greater extent, UcnI appear to act as neuromodulators in the ENS of the rat colon.

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Novel Techniques to Study Colonic Motor Function in Children

Current Gastroenterology Reports ◽

10.1007/s11894-013-0335-3 ◽

2013 ◽

Vol 15 (8) ◽

Cited By ~ 17

Author(s):

Jaime Belkind-Gerson ◽

Khoa Tran ◽

Carlo Di Lorenzo

Keyword(s):

Motor Function ◽

Colonic Motor

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VIP is involved in peripheral CRF-induced stimulation of propulsive colonic motor function and diarrhea in male rats

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00308.2017 ◽

2018 ◽

Vol 314 (5) ◽

pp. G610-G622 ◽

Cited By ~ 2

Author(s):

Seiichi Yakabi ◽

Lixin Wang ◽

Hiroshi Karasawa ◽

Pu-Qing Yuan ◽

Kazuhiko Koike ◽

...

Keyword(s):

Vasoactive Intestinal Peptide ◽

Motor Function ◽

Terminal Ileum ◽

Proximal Colon ◽

Corticotropin Releasing Factor ◽

Submucosal Plexus ◽

Myenteric Neurons ◽

Colonic Motor ◽

Fos Expression ◽

Stimulation Of

We investigated whether vasoactive intestinal peptide (VIP) and/or prostaglandins contribute to peripheral corticotropin-releasing factor (CRF)-induced CRF1 receptor-mediated stimulation of colonic motor function and diarrhea in rats. The VIP antagonist, [4Cl-D-Phe6, Leu17]VIP injected intraperitoneally completely prevented CRF (10 µg/kg ip)-induced fecal output and diarrhea occurring within the first hour after injection, whereas pretreatment with the prostaglandins synthesis inhibitor, indomethacin, had no effect. In submucosal plexus neurons, CRF induced significant c-Fos expression most prominently in the terminal ileum compared with duodenum and jejunum, whereas no c-Fos was observed in the proximal colon. c-Fos expression in ileal submucosa was colocalized in 93.4% of VIP-positive neurons and 31.1% of non-VIP-labeled neurons. CRF1 receptor immunoreactivity was found on the VIP neurons. In myenteric neurons, CRF induced only a few c-Fos-positive neurons in the ileum and a robust expression in the proximal colon (17.5 ± 2.4 vs. 0.4 ± 0.3 cells/ganglion in vehicle). The VIP antagonist prevented intraperitoneal CRF-induced c-Fos induction in the ileal submucosal plexus and proximal colon myenteric plexus. At 60 min after injection, CRF decreased VIP levels in the terminal ileum compared with saline (0.8 ± 0.3 vs. 2.5 ± 0.7 ng/g), whereas VIP mRNA level detected by qPCR was not changed. These data indicate that intraperitoneal CRF activates intestinal submucosal VIP neurons most prominently in the ileum and myenteric neurons in the colon. It also implicates VIP signaling as part of underlying mechanisms driving the acute colonic secretomotor response to a peripheral injection of CRF, whereas prostaglandins do not play a role. NEW & NOTEWORTHY Corticotropin-releasing factor (CRF) in the gut plays a physiological role in the stimulation of lower gut secretomotor function induced by stress. We showed that vasoactive intestinal peptide (VIP)-immunoreactive neurons in the ileal submucosal plexus expressed CRF1 receptor and were prominently activated by CRF, unlike colonic submucosal neurons. VIP antagonist abrogated CRF-induced ileal submucosal and colonic myenteric activation along with functional responses (defecation and diarrhea). These data point to VIP signaling in ileum and colon as downstream effectors of CRF.

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The Mental Regulation of Intestinal Activity

Journal of Mental Science ◽

10.1192/bjp.81.333.376 ◽

1935 ◽

Vol 81 (333) ◽

pp. 376-388

Author(s):

J. M. Edwards

Keyword(s):

Motor Function ◽

Habit Formation ◽

Conditional Reflex ◽

Proper Function ◽

Ménière’S Disease ◽

Rational Basis ◽

Waste Products ◽

Intestinal Activity ◽

Colonic Motor ◽

Mental Aspect

The control of the colonic motor function, and especially of the series of events which lead to defecation, is generally recognized as being a subject of the greatest importance in medicine; and, more particularly, the possibilities of varying that control. There are a large number of diseases that may, in special instances or in general, be due to constipation and inefficient elimination of waste products. Constipation has been claimed as the first step towards the different catastrophes ranging from Menière's disease and otosclerosis, gout, hyperpiesia and certain of the rheumatisms, to cases of hernia and abnormal presentation. It is my endeavour to look upon it as being even more prominently a secondary manifestation, a symptom of an even more widespread condition—mental misapplication and disorders of mental forces. With this in mind and dealing with an argument that is already proved to some degree in its most marked details, it is hoped to present, not masses of data and deduction so much as an illustration of the value, and even a hint at the frequent therapeutic necessity of orientating the various causation circles in this direction. As a cause, and especially of these mental difficulties themselves, constipation is well enough stressed; constipation as a result has not yet been sufficiently realized, nor attacked rationally from its base. The words “habit formation” cover most of the therapeutic efforts from the mental side, and that is conceived very much as a time-conditional reflex of purely physical determination. A more definite idea, then, of the mental aspect of intestinal motor function may be helpful, and especially so when so many of the habitual purgative class of drug are being authoritatively questioned as being disorganizing to this proper function. The treatment of constipation is hardly yet on a successful or rational basis.

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