Optogenetic Induction of Propagating Colonic Motor Complexes and Silencing of Colonic Motility Using Cre-Inducible Activation and Inactivation of Calretinin-Expressing Neurons

2017 ◽  
Vol 152 (5) ◽  
pp. S102 ◽  
Author(s):  
Jing Feng ◽  
Timothy J. Hibberd ◽  
Jialie Luo ◽  
Pu Yang ◽  
Nick J. Spencer ◽  
...  
Keyword(s):  
Colonic Motility ◽  
Colonic Motor ◽  
Inducible Activation

5-Hydroxytryptophan activates colonic myenteric neurons and propulsive motor function through 5-HT4 receptors in conscious mice

2007 ◽  
Vol 292 (1) ◽  
pp. G419-G428 ◽  
Author(s):  
L. Wang ◽  
V. Martínez ◽  
H. Kimura ◽  
Y. Taché
Keyword(s):  
Motor Function ◽  
Colonic Motility ◽  
Distal Colon ◽  
Nadph Diaphorase ◽  
Maximal Response ◽  
Myenteric Neurons ◽  
Diaphorase Activity ◽  
Colonic Motor ◽  
Different Populations ◽  
Fos Expression

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.

Prolonged ambulatory canine colonic motility

1995 ◽  
Vol 268 (4) ◽  
pp. G650-G662 ◽  
Author(s):  
S. M. Scott ◽  
M. A. Pilot ◽  
T. G. Barnett ◽  
N. S. Williams
Keyword(s):  
Phase 1 ◽  
Colonic Motility ◽  
Proximal Colon ◽  
Phase 3 ◽  
Postprandial Period ◽  
Long Duration ◽  
Colonic Motor ◽  
Digital Recorder ◽  
Meal Time ◽  
Low Amplitude

Canine gastrointestinal motility is studied at present in animals confined to a small cage or sling. The aims of this study were to record colonic activity over a 24-h period in eight dogs by an ambulatory method. Motility signals from implanted strain gauges were processed and stored via a portable battery-operated amplifier and digital recorder housed in a jacket. Ambulant interdigestive activity was the same as observed in laboratory experiments, with migrating colonic motor complexes (CMCs) and infrequent giant contractions (GCs). Feeding caused a multiphasic alteration in motility for 582.1 +/- 18.1 min (mean +/- SE). There were four distinct phases. During the "early" (0-2 h) postprandial period, phase 1 (mean duration: 55.1 +/- 4.0 min), which was distinguished by CMCs of high frequency and elevated amplitude in the proximal colon, and phase 2 (78.2 +/- 6.2 min), which had CMC characteristics similar to those in the interdigestive period, occurred. Phase 3 (218.8 +/- 13.6 min), a further period of increased motility, and phase 4 (339.1 +/- 14.0 min), characterized by low-amplitude long-duration CMCs, occurred during the "late" (2 h onward) postprandial response. With the exception of phase 3, postprandial phases were not always present following food intake, and their expression was markedly influenced by variations in meal time and by defecation immediately following feeding. Spontaneous defecation was characterized by a variety of motor profiles, with a GC accompanying two-thirds of episodes. We conclude that a more complete picture of canine colonic motility has been documented because of the development of the ambulatory system.

Advances in colonic motor complexes in mice

2021 ◽  
Vol 320 (1) ◽  
pp. G12-G29
Author(s):  
N. J. Spencer ◽  
M. Costa ◽  
T. J. Hibberd ◽  
J. D. Wood
Keyword(s):  
Colonic Motility ◽  
Serotonin Release ◽  
Mechanical Stimuli ◽  
Gi Tract ◽  
Mouse Colon ◽  
Colonic Motor ◽  
Large Populations ◽  
Ec Cells ◽  
Gi Motility

The primary functions of the gastrointestinal (GI) tract are to absorb nutrients, water, and electrolytes that are essential for life. This is accompanied by the capability of the GI tract to mix ingested content to maximize absorption and effectively excrete waste material. There have been major advances in understanding intrinsic neural mechanisms involved in GI motility. This review highlights major advances over the past few decades in our understanding of colonic motor complexes (CMCs), the major intrinsic neural patterns that control GI motility. CMCs are generated by rhythmic coordinated firing of large populations of myenteric neurons. Initially, it was thought that serotonin release from the mucosa was required for CMC generation. However, careful experiments have now shown that neither the mucosa nor endogenous serotonin are required, although, evidence suggests enteroendocrine (EC) cells modulate CMCs. The frequency and extent of propagation of CMCs are highly dependent on mechanical stimuli (circumferential stretch). In summary, the isolated mouse colon emerges as a good model to investigate intrinsic mechanisms underlying colonic motility and provides an excellent preparation to explore potential therapeutic agents on colonic motility, in a highly controlled in vitro environment. In addition, during CMCs, the mouse colon facilitates investigations into the emergence of dynamic assemblies of extensive neural networks, applicable to the nervous system of different organisms.

Role of adipokines in regulation of colonic motor activity in overweight and obese individuals

2021 ◽  
pp. 48-51
Author(s):  
М. М. Fedorin ◽  
M. A. Livzan ◽  
O. V. Gaus
Keyword(s):  
Literature Search ◽  
Colonic Motility ◽  
Gastrointestinal Hormones ◽  
Colonic Motor ◽  
Motility Regulation ◽  
Colonic Motor Activity ◽  
And Function ◽  
Overweight Or Obesity ◽  
Key Words Colon

The increasing proportion of the population suffering from overweight or obesity is now taking on the character of a pandemic. In the literature, there have begun to appear reports of associations in individuals with impaired colonic motility and a body mass index above 25 kg/m2. The present publication was prepared to systematize data on possible mechanisms of colonic motility disorders in overweight and obese individuals, including through changes in adipokine secretion and function. The literature search was performed in Embase, PubMed, and Google Scholar, using the key words ‘colon motility regulation’, ‘adipokines’, ‘gastrointestinal hormones’, ‘intestinal microbiota’, ‘overweight’, ‘obesity’, ‘visceral fat’.

scholarly journals Abnormal absorptive colonic motor activity in germ-free mice is rectified by butyrate, an effect possibly mediated by mucosal serotonin

2018 ◽  
Vol 315 (5) ◽  
pp. G896-G907 ◽  
Author(s):  
Alexander D. Vincent ◽  
Xuan-Yu Wang ◽  
Sean P. Parsons ◽  
Waliul I. Khan ◽  
Jan D. Huizinga
Keyword(s):  
Tryptophan Hydroxylase ◽  
Ex Vivo ◽  
Colonic Motility ◽  
Short Chain ◽  
In Vivo Studies ◽  
Striking Difference ◽  
Motor Patterns ◽  
Spatiotemporal Mapping ◽  
Germ Free ◽  
Colonic Motor

The role of short-chain fatty acids (SCFAs) in the control of colonic motility is controversial. Germ-free (GF) mice are unable to produce these metabolites and serve as a model to study how their absence affects colonic motility. GF transit is slower than controls, and colonization of these mice improves transit and serotonin [5-hydroxytryptamine (5-HT)] levels. Our aim was to determine the role SCFAs play in improving transit and whether this is dependent on mucosal 5-HT signaling. Motility was assessed in GF mice via spatiotemporal mapping. First, motor patterns in the whole colon were measured ex vivo with or without luminal SCFA, and outflow from the colon was recorded to quantify outflow caused by individual propulsive contractions. Second, artificial fecal pellet propulsion was measured. Motility was then assessed in tryptophan hydroxylase-1 (TPH1) knockout (KO) mice, devoid of mucosal 5-HT, with phosphate buffer, butyrate, or propionate intraluminal perfusion. GF mice exhibited a lower proportion of propulsive contractions, lower volume of outflow/contraction, slower velocity of contractions, and slower propulsion of fecal pellets compared with controls. SCFAs changed motility patterns to that of controls in all parameters. Butyrate administration increased the proportion of propulsive contractions in controls yet failed to in TPH1 KO mice. Propionate inhibited propulsive contractions in all mice. Our results reveal significant abnormalities in the propulsive nature of colonic motor patterns in GF mice, explaining the decreased transit time in in vivo studies. We show that butyrate but not propionate activates propulsive motility and that this may require mucosal 5-HT. NEW & NOTEWORTHY Understanding the role that the microbiota play in governing the physiology of colonic motility is lacking. Here, we offer for the first time, to our knowledge, a detailed analysis of colonic motor patterns and pellet propulsion using spatiotemporal mapping in the absence of microbiota. We show a striking difference in germ-free and control phenotypes and attribute this to a lack of fermentation-produced short-chain fatty acid. We then show that butyrate but not propionate can restore motility and that the butyrate effect likely requires mucosal 5-hydroxytryptamine.

Short-chain fatty acids modify colonic motility through nerves and polypeptide YY release in the rat

1998 ◽  
Vol 275 (6) ◽  
pp. G1415-G1422 ◽  
Author(s):  
Christine Cherbut ◽  
Laurent Ferrier ◽  
Claude Rozé ◽  
Younès Anini ◽  
Hervé Blottière ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Colonic Motility ◽  
Neural Mechanism ◽  
Short Chain Fatty Acids ◽  
Intestinal Content ◽  
Nerve Fibers ◽  
Short Chain ◽  
Motor Patterns ◽  
Colonic Motor ◽  
Chain Fatty Acids

Short-chain fatty acids (SCFAs) are recognized as the major anions of the large intestinal content in humans, but their effect on colonic motility is controversial. This study explores the colonic motor effect of SCFAs and their mechanisms in the rat. Colonic motility (electromyography) and transit time (plastic markers) were measured in conscious rats while SCFAs were infused into the colon, either alone or after administration of neural antagonists or immunoneutralization of circulating polypeptide YY (PYY). SCFA-induced PYY release was measured by RIA and then simulated by infusing exogenous PYY. Intracolonic infusion of 0.4 mmol/h SCFAs had no effect, whereas 2 mmol/h SCFAs reduced colonic motility (36 ± 3 vs. 57 ± 4 spike bursts/h with saline, P< 0.05) by decreasing the ratio of nonpropulsive to propulsive activity. This resulted in an increased transit rate ( P < 0.01). Neither α-adrenoceptor blockade nor nitric oxide synthase inhibition prevented SCFA-induced motility reduction. Intraluminal procaine infusion suppressed the SCFA effect, indicating that a local neural mechanism was involved. SCFA colonic infusion stimulated PYY release in blood. Immunoneutralization of circulating PYY abolished the effect of SCFAs on colonic motility, whereas exogenous PYY infusion partly reproduced this effect. SCFAs modify colonic motor patterns in the rat and increase transit rate; local nerve fibers and PYY are involved in this effect.

Changes in colonic motility following abdominal irradiation in dogs

1993 ◽  
Vol 264 (6) ◽  
pp. G1024-G1030 ◽  
Author(s):  
R. W. Summers ◽  
B. Hayek
Keyword(s):  
Colonic Motility ◽  
Mean Amplitude ◽  
X Rays ◽  
Motor Patterns ◽  
Colonic Motor ◽  
Before And After ◽  
Irradiation Dosage ◽  
The Mean ◽  
Giant Migrating Contractions

The purpose of the study was to compare colonic motor patterns before and after a single abdominal dose of X-rays in dogs. Recordings were made from five serosally implanted strain gauges at equidistant intervals along the colon in seven dogs (2 dogs also had 2 jejunal electrodes and 1 had ileal electrodes). Control recordings were made for 3 h in the fasted state and daily for 2 wk after an absorbed X-ray dose of 938 cGy was delivered to the abdomen. The duration of migrating colonic motor complexes decreased from 7.2 +/- 0.5 to 3.9 +/- 0.4 min while the mean amplitude fell from 10.3 +/- 0.6 to 1.8 +/- 0.2 g (P < 0.05). The rate of nonmigrating colonic motor complex occurrence increased from 0.6 +/- 0.1 to 1.2 +/- 0.2 per hour (P < 0.05). Colonic giant migrating contractions were rarely observed during control recordings (2 in 80 h of recording). In contrast, repetitive clusters of giant contractions were observed 5-8 days after exposure in five of seven dogs (1.5/h) and were associated with restlessness, whining, and passage of diarrheal stools (sometimes bloody) with nearly every occurrence. The basic colonic motility patterns were less disrupted than were jejunal myoelectric patterns at the same irradiation dosage. However, the study demonstrates the important role of colonic giant migrating contractions in pathological diarrheal states such as irradiation injury.

Induction of postprandial intestinal motility and release of cholecystokinin by polyamines in rats

1994 ◽  
Vol 267 (6) ◽  
pp. G960-G965
Author(s):  
J. Fioramonti ◽  
M. J. Fargeas ◽  
V. Bertrand ◽  
L. Pradayrol ◽  
L. Bueno
Keyword(s):  
Intestinal Motility ◽  
Day Treatment ◽  
Colonic Motility ◽  
Burst Frequency ◽  
Spike Burst ◽  
Colonic Motor ◽  
Saline Administration ◽  
Induce Change ◽  
Spike Bursts ◽  
Cck Release

Polyamines are known to play a major role in postprandial adaptation of the digestive tract. Experiments were designed to determine whether ingested polyamines induce change in intestinal motility associated with a cholecystokinin (CCK) release and whether endogenous polyamines are involved in the intestinal and colonic motor response to a meal. Intestinal and colonic motility was assessed in rats equipped with intestinal electrodes, and plasma CCK was determined using a bioassay. Orogastric administration of putrescine, spermidine, or spermine (20 mumol) disrupted intestinal migrating myoelectric complexes (MMCs) and increased the frequency of colonic spike bursts. After a 6-day treatment with the ornithine decarboxylase inhibitor alpha-difluoromethylornithine, the duration of postprandial disruption of MMCs, but not the stimulation of colonic motility, induced by a 3-g meal was significantly reduced. The duration of MMC disruption and the increase in colonic spike burst frequency after spermidine administration (20 mumol) were significantly reduced by CCK-A and CCK-B antagonists. Eight minutes after saline administration plasma CCK concentration was 0.9 +/- 0.4 pM; it rose to 4.7 +/- 2.8 pM, 8 min after spermidine (20 mumol). These results indicate that exogenous polyamines disrupt intestinal MMCs and stimulate colonic motility through a release of CCK acting at CCK-A and CCK-B receptors and suggest that endogenous polyamines are involved in the postprandial control of intestinal motility.

Effects of a cannabinoid receptor agonist on colonic motor and sensory functions in humans: a randomized, placebo-controlled study

2007 ◽  
Vol 293 (1) ◽  
pp. G137-G145 ◽  
Author(s):  
Tuba Esfandyari ◽  
Michael Camilleri ◽  
Irene Busciglio ◽  
Duane Burton ◽  
Kari Baxter ◽  
...  
Keyword(s):  
Cannabinoid Receptors ◽  
Diarrheal Disease ◽  
Cannabinoid Receptor ◽  
Colonic Motility ◽  
Cholinergic Neurons ◽  
Controlled Study ◽  
Double Blind ◽  
Colonic Motor ◽  
Irritable Bowel ◽  
The Brain

Cannabinoid receptors (CBR) are located on cholinergic neurons in the brain stem, stomach, and colon. CBR stimulation inhibits motility in rodents. Effects in humans are unclear. Dronabinol (DRO), a nonselective CBR agonist, inhibits colonic motility and sensation. The aim of this study was to compare effects of DRO and placebo (PLA) on colonic motility and sensation in healthy volunteers. Fifty-two volunteers were randomly assigned (double-blind) to a single dose of 7.5 mg DRO or PLA postoperative with concealed allocation. A balloon-manometric assembly placed into the descending colon allowed assessment of colonic compliance, motility, tone, and sensation before and 1 h after oral ingestion of medication, and during fasting, and for 1 h after 1,000-kcal meal. There was an overall significant increase in colonic compliance ( P = 0.045), a borderline effect of relaxation in fasting colonic tone ( P = 0.096), inhibition of postprandial colonic tone ( P = 0.048), and inhibition of fasting and postprandial phasic pressure ( P = 0.008 and 0.030, respectively). While DRO did not significantly alter thresholds for first gas or pain sensation, there was an increase in sensory rating for pain during random phasic distensions at all pressures tested and in both genders ( P = 0.024). In conclusion, in humans the nonselective CBR agonist, DRO, relaxes the colon and reduces postprandial colonic motility and tone. Increase in sensation ratings to distension in the presence of relaxation of the colon suggests central modulation of perception. The potential for CBR to modulate colonic motor function in diarrheal disease such as irritable bowel syndrome deserves further study.

scholarly journals Cholinergic giant migrating contractions in conscious mouse colon assessed by using a novel noninvasive solid-state manometry method: modulation by stressors

2009 ◽  
Vol 296 (5) ◽  
pp. G992-G1002 ◽  
Author(s):  
G. Gourcerol ◽  
L. Wang ◽  
D. W. Adelson ◽  
M. Larauche ◽  
Y. Taché ◽  
...  
Keyword(s):  
High Frequency ◽  
Colonic Motility ◽  
Distal Colon ◽  
High Amplitude ◽  
Corticotrophin Releasing Factor ◽  
Colonic Manometry ◽  
Colonic Motor ◽  
Chronic Stressors ◽  
Giant Migrating Contractions

There is a glaring lack of knowledge on mouse colonic motility in vivo, primarily due to unavailability of adequate recording methods. Using a noninvasive miniature catheter pressure transducer inserted into the distal colon, we assessed changes in colonic motility in conscious mice induced by various acute or chronic stressors and determined the neurotransmitters mediating these changes. Mice exposed to restraint stress (RS) for 60 min displayed distal colonic phasic contractions including high-amplitude giant migrating contractions (GMCs), which had peak amplitudes >25 mmHg and occurred at a rate of 15–25 h−1 of which over 50% were aborally propagative. Responses during the first 20-min of RS were characterized by high-frequency and high-amplitude contractions that were correlated with defecation. RS-induced GMCs and fecal pellet output were blocked by atropine (0.5 mg/kg ip) or the corticotrophin releasing factor (CRF) receptor antagonist astressin-B (100 μg/kg ip). RS activated colonic myenteric neurons as shown by Fos immunoreactivity. In mice previously exposed to repeated RS (60 min/day, 14 days), or in transgenic mice that overexpress CRF, the duration of stimulation of phasic colonic contractions was significantly shorter (10 vs. 20 min). In contrast to RS, abdominal surgery abolished colonic contractions including GMCs. These findings provide the first evidence for the presence of frequent cholinergic-dependent GMCs in the distal colon of conscious mice and their modulation by acute and chronic stressors. Noninvasive colonic manometry opens new venues to investigate colonic motor function in genetically modified mice relevant to diseases that involve colonic motility alterations.

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