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.

CNS vasopressin mediates emotional stress and CRH-induced colonic motor alterations in rats

1992 ◽  
Vol 262 (3) ◽  
pp. G427-G431 ◽  
Author(s):  
L. Bueno ◽  
M. Gue ◽  
C. Delrio
Keyword(s):  
Emotional Stress ◽  
Conditioned Fear ◽  
Control Period ◽  
Colonic Motility ◽  
Burst Frequency ◽  
Spike Burst ◽  
Implanted Electrodes ◽  
Colonic Motor ◽  
The Central Nervous System ◽  
Spike Bursts

The effects of emotional stress (ES) corresponding to conditioned fear on colonic motility and its antagonism by [deamino-Pen1, Val4, D-Arg8]vasopressin, a vasopressin antagonist, were investigated by electromyography in conscious fasted rats fitted with chronically implanted electrodes. A 117% increase (19.6 +/- 2.1 vs. 9.0 +/- 0.9 cycles/10 min during the control period) in the frequency of colonic spike bursts was observed when rats were placed for 30 min in a box in which they had previously received electric foot shocks. Intracerebroventricular (icv) administration of corticotropin-releasing hormone (CRH; 0.5 micrograms/kg) mimicked the effects of ES and increased the spike burst frequency of the colon by 88.6% from 5 to 15 min after its administration. At doses between 5 and 20 micrograms/kg the antagonist [deamino-Pen1, Val4, D-Arg8]vasopressin significantly reduced or abolished the effects of ES and CRH administration on colonic motility. Injected icv at doses of 2.5 and 5 ng/kg [Arg8]vasopressin dose dependently increased the frequency of colonic spike bursts. These effects were not reproduced by similar or higher (50 ng/kg) doses given intraperitoneally, and the effects were abolished after previous administration of vasopressin at a dose of 20 micrograms/kg. It is concluded that the effects of ES on colonic motility in rats previously shown to be linked to the central nervous system (CNS) release of CRH are in turn mediated through the central release of vasopressin.

Longitudinal and circumferential spread of spike bursts in canine jejunum in vivo

1980 ◽  
Vol 239 (4) ◽  
pp. G311-G318 ◽  
Author(s):  
N. S. Dusdieker ◽  
R. W. Summers
Keyword(s):  
Phase Ii ◽  
Slow Wave ◽  
Intestinal Motility ◽  
New Method ◽  
Phase Iii ◽  
Cross Sectional ◽  
Spike Burst ◽  
Healthy Dogs ◽  
Spike Bursts

This study demonstrates a new method for quantitatively analyzing individual intestinal spike bursts and establishes the distribution of spike burst spread under conditions of fasting and feeding in conscious healthy dogs. The dimensions and propagation lengths of individual jejunal spike bursts were determined by studying spike burst spread within slow-wave cycles. Electromyograms were recorded simultaneously from multiple closely spaced serosal electrodes in the jejunum (4 equally distant around the circumference and 16 along the long axis at 3-cm intervals). At least 75% of the time, spike bursts involved the entire cross-sectional circumference simultaneously. Greater than 50% of spike bursts during fasting or feeding spread distally 3-30 cm. The remainder were isolated or segmental spike bursts involving < 3 cm of jejunum. The lengths of propagative spike bursts increased with the time during phase II and reached a maximum of 30-40 cm during phase III. Fed activity showed a mixture of segmental and longer propagative spike bursts that varied little with time after feeding. Propagative spike bursts > 3 cm in length produced at least 85% of the total myoelectric burst activity regardless of the state of fasting or feeding and constitute the major form of intestinal motility in the canine jejunum.

Changes in jejunal myoelectrical activity during exercise in fed untrained dogs

1988 ◽  
Vol 254 (5) ◽  
pp. G741-G747
Author(s):  
M. J. Kenney ◽  
A. Flatt ◽  
R. W. Summers ◽  
C. K. Brown ◽  
C. V. Gisolfi
Keyword(s):  
Gastrointestinal Symptoms ◽  
Proximal Jejunum ◽  
Regular Spike ◽  
Short Term ◽  
Burst Frequency ◽  
Myoelectrical Activity ◽  
Spike Burst ◽  
Bipolar Electrodes ◽  
Exercise Induced ◽  
Spike Bursts

Seven female dogs (15-20 kg) were instrumented with seven bipolar electrodes sutured at 3-cm intervals to the serosal surface of the proximal jejunum and were exercised at different intensities and durations on a motor-driven treadmill. Slow-wave frequency increased (P less than 0.05) from preexercise control during prolonged (90 min) exercise and during recovery after short-term exercise (30 min) at 70% heart rate reserve (HRR). These changes were associated with an increase in core temperature. Spike-burst frequency (SBF) increased (P less than 0.05) with moderate exercise (50% HRR), but the magnitude was small. When exercise was extended beyond 30 min and during all recovery periods, SBF decreased significantly. Exercise produced migrating myoelectrical complexes in three experiments and less dramatic pattern changes characterized as "clustered contractions" (regular spike bursts preceded and followed by the absence of spike bursts) in at least nine other experiments. We conclude that exercise does alter jejunal myoelectrical activity, but myoelectrical patterns may be more important in explaining exercise-induced gastrointestinal symptoms than changes in spike-burst frequency or duration.

Interaction between CCK and opioids in the modulation of the rectocolonic inhibitory reflex in rats

1995 ◽  
Vol 269 (2) ◽  
pp. G240-G245
Author(s):  
M. Gue ◽  
C. del Rio ◽  
J. L. Junien ◽  
L. Bueno
Keyword(s):  
Colonic Motility ◽  
Proximal Colon ◽  
Blocking Effect ◽  
Motor Inhibition ◽  
Rectal Distension ◽  
Cholecystokinin Receptors ◽  
Colonic Motor ◽  
The Brain ◽  
Spike Bursts ◽  
Inhibitory Reflex

The effects of cholecystokinin octapeptide (CCK-8) as well as the involvement of opioid system were evaluated in rectal distension (RD)-induced colonic motor inhibition in rats. Rats were surgically prepared with electrodes implanted on the proximal colon, and a catheter was implanted in lateral ventricle of the brain. RD was performed by inflation (0.0-1.6 ml) of a balloon rectally inserted. RD 1.6 ml of induced an inhibition of the colonic spike bursts (3.1 +/- 0.5 per 5 min vs. 8.1 +/- 0.4 before RD). Intracerebroventricular but not intravenous injection of CCK-8 and A-71623 (50 and 100 ng/kg) reduced the RD-induced colonic motor inhibition, whereas A-63387 was ineffective. PD-135,158 (10 micrograms/kg icv) suppressed the inhibitory reflex caused by RD. Devazepide (100 micrograms/kg icv) had no effect in this reflex function. Devazepide (1 microgram/kg), naloxone (0.1 mg/kg), and nor-binaltorphimine (nor-BNI; 10 mg/kg) reversed the blocking effect of CCK-8, whereas PD-135,158 (0.1 microgram/kg) and naltrindole (1 mg/kg) have no effect. In conclusion, CCK-8 acts on central alimentary cholecystokinin receptors to modulate the RD-induced inhibition of colonic motility through pathways involving activation of endogenous kappa-receptors.

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.

Stimulation of duodenal motility by hyperosmolar mannitol depends on local osmoreceptor control

1994 ◽  
Vol 266 (5) ◽  
pp. G940-G943 ◽  
Author(s):  
H. C. Lin ◽  
J. D. Elashoff ◽  
G. M. Kwok ◽  
Y. G. Gu ◽  
J. H. Meyer
Keyword(s):  
Intestinal Motility ◽  
Control Mechanism ◽  
Experimental Methods ◽  
Dose Effect ◽  
Duodenal Motility ◽  
Significant Difference ◽  
Intestinal Distension ◽  
Osmotic Equilibration ◽  
Spike Bursts ◽  
Stimulation Of

Duodenal motility is stimulated by hyperosmolar solution. Since intestinal distension also stimulates intestinal motility, this increase in the motility response may be due to either stimulation of duodenal local osmoreceptor control or intestinal distension resulting from osmotic equilibration. To test which mechanism is primarily responsible for this osmotically sensitive effect, we compared the number of duodenal spike bursts in five dogs equipped with duodenal fistulas that allowed for the preservation or removal of intestinal distension. The response to 300 vs. 1,200 mosM mannitol was compared under three experimental perfusion methods: 1) distension was preserved both proximal and distal to the fistula (DD); 2) distension proximal to the fistula was removed (rD); and 3) distension both proximal and distal to the fistula was removed (rr). The test solutions had access to either the whole gut (DD and rD) or only the first 10 cm of the duodenum (rr). We found that 1) there were more spike bursts after the hyperosmolar solution (dose effect, P < 0.05, analysis of variance); 2) there was no significant difference between the three experimental methods; and 3) the stimulating effect of hyperosmolar solution depended on the first 10 cm of the duodenum. Thus, since hyperosmolar solution increased duodenal motility regardless of whether intestinal distension was preserved or removed, the stimulating effect of hyperosmolar solution on duodenal motility was primarily the result of a local osmoreceptor control mechanism located in the first 10 cm of the duodenum.

scholarly journals Persistent Na+ Current Modifies Burst Discharge By Regulating Conditional Backpropagation of Dendritic Spikes

2003 ◽  
Vol 89 (1) ◽  
pp. 324-337 ◽  
Author(s):  
Brent Doiron ◽  
Liza Noonan ◽  
Neal Lemon ◽  
Ray W. Turner
Keyword(s):  
Sodium Current ◽  
Pyramidal Cells ◽  
Weakly Electric Fish ◽  
Burst Frequency ◽  
Burst Discharge ◽  
Dendritic Spikes ◽  
Dendritic Spike ◽  
Time Required ◽  
Weakly Electric ◽  
Spike Bursts

The estimation and detection of stimuli by sensory neurons is affected by factors that govern a transition from tonic to burst mode and the frequency chracteristics of burst output. Pyramidal cells in the electrosensory lobe of weakly electric fish generate spike bursts for the purpose of stimulus detection. Spike bursts are generated during repetitive discharge when a frequency-dependent broadening of dendritic spikes increases current flow from dendrite to soma to potentiate a somatic depolarizing afterpotential (DAP). The DAP eventually triggers a somatic spike doublet with an interspike interval that falls inside the dendritic refractory period, blocking spike backpropagiation and the DAP. Repetition of this process gives rise to a rhythmic dendritic spike failure, termed conditional backpropagation, that converts cell output from tonic to burst discharge. Through in vitrorecordings and compartmental modeling we show that burst frequency is regulated by the rate of DAP potentiation during a burst, which determines the time required to discharge the spike doublet that blocks backpropagation. DAP potentiation is maginfied through a postitve feedback process when an increase in dendritic spike duration activates persistent sodium current ( I NaP). I NaP further promotes a slow depolarization that induces a shift from tonic to burst discharge over time. The results are consistent with a dynamical systems analysis that shows that the threshold separating tonic and burst discharge can be represented as a saddle-node bifurcation. The interaction between dendritic K+ current and I NaP provides a physiological explanation for a variable time scale of bursting dynamics characteristic of such a bifurcation.

scholarly journals Spike interval coding of translatory optic flow and depth from motion in the fly visual system

2016 ◽  
Author(s):  
Kit D. Longden ◽  
Martina Wicklein ◽  
Benjamin J. Hardcastle ◽  
Stephen J. Huston ◽  
Holger G. Krapp
Keyword(s):  
Optic Flow ◽  
Visual Processing ◽  
Visual Motion ◽  
Receptive Fields ◽  
Cell Types ◽  
Spike Burst ◽  
Cluttered Environments ◽  
Single Spike ◽  
Self Motion ◽  
Spike Bursts

SummaryMany animals use the visual motion generated by travelling in a line, the translatory optic flow, to successfully navigate obstacles: near objects appear larger and to move more quickly than distant ones. Flies are experts at navigating cluttered environments, and while their visual processing of rotatory optic flow is understood in exquisite detail, how they process translatory optic flow remains a mystery. Here, we present novel cell types that have motion receptive fields matched to translation self-motion, the vertical translation (VT) cells. One of these, the VT1 cell, encodes forwards sideslip self-motion, and fires action potentials in clusters of spikes, spike bursts. We show that the spike burst coding is size and speed-tuned, and is selectively modulated by parallax motion, the relative motion experienced during translation. These properties are spatially organized, so that the cell is most excited by clutter rather than isolated objects. When the fly is presented with a simulation of flying past an elevated object, the spike burst activity is modulated by the height of the object, and the single spike rate is unaffected. When the moving object alone is experienced, the cell is weakly driven. Meanwhile, the VT2-3 cells have motion receptive fields matched to the lift axis. In conjunction with previously described horizontal cells, the VT cells have the properties required for the fly to successfully navigate clutter and encode its movements along near cardinal axes of thrust, lift and forward sideslip.

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.

The specific long spike burst pattern indicates the presence of regional variability in the ovine gallbladder motor function

Biologia ◽  
2017 ◽  
Vol 72 (12) ◽  
Author(s):  
Krzysztof Romański ◽  
Józef Nicpoń
Keyword(s):  
Small Bowel ◽  
Phase 1 ◽  
Force Transducer ◽  
Specific Pattern ◽  
Regional Variability ◽  
Burst Frequency ◽  
Myoelectrical Activity ◽  
Spike Burst ◽  
Burst Pattern ◽  
Rhythm Pattern

AbstractThe myoelectrical activity of ovine gallbladder is incompletely recognized. Accordingly, each of five rams was fitted with six small intestinal and three gallbladder electrodes. The strain gauge force transducer was also mounted near the gallbladder fundic electrode. In two series of chronic experiments the electromyographical and mechanical recordings were conducted during 5–7 h in fasted or non-fasted animals, with or without feeding. The occurrence of the slow waves in the small bowel was common, unlike those in the gallbladder. In the small bowel myoelectrical records both the migrating motility complex and minute rhythm pattern were observed regularly. In the gallbladder, both the migrating motility complex-like activity and the minute rhythm were also denoted in the same time as in the small bowel. In gallbladder infundibulum, and often also in the gallbladder corpus, the specific pattern, called the long spike burst pattern (LSBP) was observed. It comprised usually one or two parts of prolonged duration. The first part resembled the classical (short lasting) spike burst in the small bowel and its amplitude was lower than that of the second part. The spike burst frequency of the second part of the pattern was 2–3 times lower than that of the first part. During phase 1 – and phase 2a-like activity, the frequency of the gallbladder LSBP was reduced in fasted rams. The LSBP amplitude was relatively high and not further enhanced after feeding. In fasted rams, the duration of specific pattern, observed in gallbladder infundibulum, was longer than that in non-fasted animals and its amplitude was low. Similar events were recorded in the gallbladder corpus, but the LSBP was shorter and not regular. In the gallbladder fundus, mostly irregular short spike bursts were recorded. It is concluded that in sheep, specific types of the long-lasting groups of spikes occur in the upper gallbladder areas forming the specific pattern that indicates the presence of the regional variability of the gallbladder motor activity. The character of LSBP depends mostly on feeding conditions.

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