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PubMed2005

[Effects of intrahippocampal microinjection of motilin on interdigestive migrating myoelectrical complexes of rat duodenum].

OBJECTIVE: To explore the effects of intrahippocampal injection of motilin on interdigestive migrating myoelectrical complex (MMC) of rat duodenum. METHODS: Adult SD rats of either sex were subjected to injection of 0.5 microl motilin (0.74 nmol/microl) through the guiding cannula stereotaxically implanted into the hippocampus previously. Interdigestive MMC of the duodenum was recorded by RM6240B multilead physiological recording system. RESULTS: After motilin injection into the hippocampus, duodenal MMC cycle was significantly shortened, but the amplitude and frequency of phase III were increased without affecting the duration of phase III. The effect of motilin injection into the hippocampus on MMC was completely abolished by subdiaphragmal vagotomy but not affected by intravenously injected atropine, phentolamine or propranolol. Anti-motilin serum could partly abolish the effects of motilin on MMC. CONCLUSIONS: Motilin injection into the hippocampus have effects on the duration of duodenal MMC cycle and the amplitude and frequency of phase III, which may rely on the effect of noncholinergic and nonadrenergic neurons on duodenal smooth muscle or the increase of local motilin via hippocampus-hypothalamus-brain stem-vagus pathway. The hippocampus plays an important role in duodenal MMC.

Animals↗
PubMed1981

Intrinsic nervous control of migrating myoelectric complexes.

The role of intrinsic nerves in the control of migrating myoelectric complexes (MMCs) was studied in seven conscious dogs, each implanted with a set of eight bipolar Trimel wire electrodes. Local areas, 3-5 cm long, were perfused close intra-arterially via an exteriorized heparinized Silastic cannula. Experiments consisted of giving bolus injections of atropine (20-50 micrograms), hexamethonium (20 mg), and tetrodotoxin (TTX; 3-30 micrograms) via the catheter at varying periods of time with respect to the arrival of phase III at the perfused site. Atropine and hexamethonium, given close intra-arterially immediately before the arrival of phase II at the perfused site, blocked its further propagation. Tetrodotoxin given locally also blocked the propagation of phage III, as above. After the block, TTX initiated a new phase III activity at, or distal to, the perfused site in 10 out of 14 perfusions. The new phase III activity propagated distally. This study shows that the mechanisms for the initiation and propagation of MMCs are built into the enteric plexus. Once an MMC is initiated, its propagation is achieved by proximal-to-distal excitation through the intrinsic cholinergic network of neurons. This study explains the lack of any significant changes in the propagation parameters of MMCs after vagotomy or celiac and superior mesenteric ganglionectomy.

Animals↗
PubMed1985

Dose- and time-dependent biphasic response to morphine on intestinal migrating myoelectric complex.

We investigated the biphasic response to morphine infusion on migrating myoelectric complex (MMC) cycling in seven conscious dogs. Morphine infusions at the rate of 20, 50, 100, 200, 500 and 1000 micrograms/kg/hr were started at 0 or 40% of MMC cycle and continued for 3 hr in each experiment. All infusion rates starting at 40% of MMC cycle initiated the first postinfusion MMC cycle prematurely (P less than .05). The mean period of the first postinfusion MMC cycle decreased for higher infusion rates. After the first premature MMC cycle, higher infusion rates (500 and 1000 micrograms/kg/hr) inhibited MMC cycling completely whereas the lower infusion rates inhibited MMC cycling in a dose-dependent manner. When infusion was started at 0% of MMC cycle, the first premature MMC cycle occurred consistently only at 20 micrograms/kg/hr. For higher infusion rates, initiation of premature MMC cycle or inhibition of MMC cycling was dose-dependent. Naloxone blocked both the excitatory and the inhibitory effects of morphine on MMC cycling. Morphine infusions also initiated phase III activity in the postprandial state in a dose-dependent manner. Truncal vagotomy and splanchnectomy did not abolish the excitatory or the inhibitory effects of morphine on MMC cycling. We conclude that morphine infusion has a biphasic effect on MMC cycling. The exact nature of the response depends on the dose of morphine and the time in the MMC cycle when infusion is started. Both the excitatory and the inhibitory responses may be mediated through peripheral mu opiate receptors.

Animals↗
PubMed1995

Is nitric oxide the final mediator regulating the migrating myoelectric complex cycle?

The main objective was to study the role of nitric oxide (NO) in the conversion of migrating myoelectric complexes (MMC) to the irregular electrical activity characteristic of the postprandial state. Both rats and chickens were implanted with electrodes for electromyography in the small intestine. Intravenous infusion of NG-nitro-L-arginine (L-NNA), a NO synthase inhibitor, induced an organized MMC-like pattern in fed rats. Infusion of sodium nitroprusside, a NO donor, disrupted the MMC, inducing a postprandial-like motor pattern in fasting rats. Similarly, in chickens L-NNA mimicked the fasting pattern, consisting of a shortening of phase II, enlargement of phase III, orad displacement of the origin of the MMC, and an increase in the speed of phase III propagation. An inhibition of NO synthesis seems to be involved in the induction of the fasting motor pattern, whereas an increase of NO mediates the occurrence of the fed pattern. It is suggested that NO might be the final mediator in the control of small intestine motor patterns.

Amino Acid Oxidoreductases↗
PubMed1990

[The effect of microinjections of bombesin into the amygdala on the slow-wave frequency of the gastroduodenal smooth muscles and on the migrating myoelectric complex].

In dogs with electrodes implanted in the smooth muscle wall of the stomach and duodenum, microinjection of bombesin (5 micrograms) during the 2nd phase of the migrating myoelectric complex decreased frequency of slow waves in the stomach, leaving unaltered the frequency of slow waves in the duodenum. Bombesin caused a short-term inhibition of the gastric and intestinal spike activity followed by its increase, the active period of the migrating myoelectric complex being prolonged.

Amygdala↗
PubMed1995

Modulation of the migrating myoelectric complexes by cholecystokinin and gastrin in the gastrointestinal tract of chickens.

Several mammalian avian species, including the chicken, show migrating myoelectric complexes (MMC) both in unfed and fed states. In these species, postprandial hormones seem to modulate but not to disrupt the MMC. To gain more information in this modulatory role, we evaluated the role of cholecystokinin (CCK) vs gastrin on the regulation of intestinal motility in chickens. Birds were implanted with eight electrodes for electromyography in the stomach, duodenum, jejunum, and ileum. In feed-deprived animals, CCK infusion (10(-12) mol/kg per min x 3 h) did not disrupt the MMC but induced changes in the MMC pattern similar to those induced by a meal. Infusion of CCK in fed animals induced dose-dependent effects: CCK infused at 10(-11) and 3 x 10(-11) mol/kg per min x 2 h, progressively elongated the MMC and slowed the speed of propagation of Phase 3. Furthermore, CCK infused at 10(-10) mol/kg per min x 2 h disrupted the MMC but a Phase 3 appeared just after the end of the infusion. By contrast, chicken gastrin (10(-10) mol/kg per min x 2 h) did not modify the MMC pattern. In conclusion, CCK influence on the intestinal motility of chickens ranges from the modulation of the MMC to total disruption, depending on the dose. Moreover, this study suggests that the mechanism of action of CCK could be similar in both mammalian and avian small intestines.

Animals↗
PubMed1992

The role of migrating myoelectric complexes in the regulation of digesta transport in the preruminant calf.

Four calves were equipped with an electromagnetic flow probe inside the transverse duodenum and with electrodes at intervals of 2 cm on either side of the probe. Amounts of 0.5, 2.0, 3.5, and 5.0 kg of whole milk were given according to a latin square design. Recordings of digesta flow and myoelectric activity were made during a 5.6-h period after feeding to quantify the influence of migrating myoelectric complexes on digesta flow through the transverse duodenum of preruminant calf under different levels of milk intake. Immediately after feeding, a phase of irregular spiking activity appeared; its length increasing linearly (p = 0.002) with the amount of milk fed. Increasing milk intake led to linear increases in duration (p = 0.001) and total electrical activity (p = 0.002) of the irregular activity phases, quadratic shortening of the quiescent phases (p = 0.021), and linear decrease (p = 0.006) in the numbers of migrating myoelectric complexes. Intermittent flows of digesta, each of them corresponding to a strong spike burst, appeared during irregular spiking activity phases. Augmentation of the milk ingested did not affect the volume of each gush of digesta but caused a cubic increase in the number of gushes (p = 0.023) and in the total volume of digesta (p = 0.009). These cubic effects implied that with increased intake of milk, the duodenum endeavoured to accelerate the flow of digesta in an attempt to return to an "empty state" in about the same time for all levels of milk consumed. This was achieved mainly through adjustments in the duration and activity of the irregular spiking activity phase.

Animals↗
PubMed1999

Serotonin stimulates migrating myoelectric complex via 5-HT3-receptors dependent on cholinergic pathways in rat small intestine.

We have investigated the effect of 5-hydroxytryptamine (5-HT) and different 5-HT-receptor antagonists and atropine on the migrating myoelectric complex in the rat small intestine. Infusion of 5-HT dose-dependently shortened the interval between phase III of the migrating myoelectric complex (MMC). In untreated animals the interval in upper jejunum was 19.1 (16.0-22.1) min. At doses of 10 and 20 nmol kg-1 min-1, the interval decreased to 15.2 (12.0-18.4) and 10.2 (9.4-11.0) min, respectively. The 5-HT3-receptor antagonist ondansetron (0.5 mg kg-1) alone increased the MMC interval from 20.8 (15.1-26.5) to 33.9 (19.4-48.4) min. Neither methiothepin (0.5 mg kg-1) nor ketanserin (0.5 mg kg-1), selective for 5-HT1/5-HT2- and 5-HT2-receptors, respectively, changed the MMC interval. The 5-HT4-receptor antagonist GR 113808 (0.5 mg kg-1) disrupted the MMC and induced irregular spiking activity. Ondansetron and atropine antagonized the 5-HT-induced shortening of the MMC interval. Neither methiothepin nor ketanserin affected the response to 5-HT. GR 113808 did not block the response to 5-HT in half of the animals; however, in the remaining ones MMC was disrupted and irregular spiking induced. In conclusion, these results show that 5-HT dose-dependently stimulates the cycling of the MMC in the small intestine via 5-HT3-receptors and a cholinergic final pathway. Our findings encourage further studies on the role of the 5-HT3-receptor in the control of gastrointestinal motility.

Animals↗
PubMed1994

Intestinal microflora stimulates myoelectric activity of rat small intestine by promoting cyclic initiation and aboral propagation of migrating myoelectric complex.

Microbial modulation of myoelectric activity in small intestine was studied. Germ-free male Sprague-Dawley rats were equipped with bipolar electrodes from the duodenojejunal junction to the midpoint of small intestine. Prior to and one week after introduction of conventional intestinal microflora, 32 +/- 5% and 61 +/- 5% (mean +/- SE), respectively, of activity fronts of the migrating myoelectric complex reached the midpoint (P < 0.05), and the interval between activity fronts in proximal jejunum was reduced from 31.2 +/- 2.0 min to 17.5 +/- 0.8 min, respectively (P < 0.01). The pattern of propagation was more regular after conventionalization. Slow-wave frequency in proximal jejunum was 38.5 +/- 1.2/min in germ-free rats and 43.0 +/- 0.8/min in conventional rats (P < 0.01), but introduction of microflora failed to increase the frequency in germ-free rats. The frequency of spike potentials succeeding jejunal infusion of 5 ml of 12.5% glucose remained unchanged after conventionalization. Statistical analyses showed that the interval between activity fronts varied mainly within rats, whereas the propagation velocity showed statistically significant variability between rats (P < 0.01), regardless of intestinal microflora. Luminal control by the resident microflora is important for physiological cycling and aboral propagation of the migrating myoelectric complex, but seems to be of no major consequence for postprandial myoelectric response.

Action Potentials↗
PubMed1991

Modulation of the migrating myoelectric complex by brain noradrenergic systems in rats.

The respective role of central and peripheral noradrenergic systems in the control of migrating myoelectric complex (MMC) was investigated in rats following lesions with 6-hydroxydopamine (6-OHDA). 6-OHDA was injected via intraperitoneal (ip), intracisternal (icis), and intracerebroventricular (icv) routes in rats. Control animals received the vehicle alone. One month later, MMC was recorded in conscious rats chronically fitted with electrodes. The MMC period was significantly lengthened after 6-OHDA ip or icv injection, and slightly shortened after 6-OHDA icis injection. No disruption of central noradrenergic systems was detected after ip lesions. Norepinephrine content was reduced in the digestive tract after ip lesions, in the spinal cord after icis lesions, and in the cortex, the hypothalamus, pons-medulla, and the spinal cord after icv lesions. After icis lesions, noradrenergic perikarya were spared in pons-medulla, whereas only pons noradrenergic perikarya were lesioned after icv lesions. We conclude that lesions of brain noradrenergic systems modify MMC periodicity in rats. The rostral noradrenergic systems may play the major modulatory role.

Animals↗
PubMed1983

Morphine versus motilin in the initiation of migrating myoelectric complexes.

The roles of morphine and motilin in the initiation of migrating myoelectric complex (MMC) cycles were studied in four conscious dogs. Morphine or motilin boluses and morphine or motilin infusions were administered to healthy conscious dogs, each implanted with a set of 12 electrodes on the small intestine. The durations of premature phase IIIs initiated by morphine and motilin were not significantly different from each other or from control values. The premature phase IIIs initiated by morphine boluses propagated significantly faster over the 1st half of small intestine than the control or motilin bolus-initiated phase IIIs. The latent period for the onset of phase IIIs after morphine was not significantly different from that after motilin. Morphine infusion (50 micrograms X kg-1 X h-1) generally initiated one or two premature MMC cycles and then disrupted further MMC cycling. Motilin infusion (0.3 microgram X kg-1 X h-1) initiated one premature MMC cycle, and then further cycling continued at the normal rate. We conclude that morphine acts on both the MMC-initiating and MMC-propagating mechanisms, whereas motilin acts only on the MMC-initiating mechanism. Morphine has both excitatory and disruptive effects on MMC cycling, while motilin has only excitatory effects.

Animals↗
PubMed2006

[Effects of intra-amygdaloid injection of motilin on the interdigestive migrating myoelectrical complex in rat].

OBJECTIVE: This study is undertaken to explore the effects of motilin in the amygdaloid nucleus on the interdigestive migrating myoelectrical complex (MMC) in rats. METHODS: Adult SD rats of either sex were used. 0.5 microL motilin (0.74 nmol/microL) was injected into the guide cannula which had been stereotaxically implanted into the amygdaloid nucleus. Then the MMC was recorded by an RM6240B multilead physiological recording system. Some rats also received subdiaphragmatic vagotomy, or intravenous injection of the M-cholinergic receptor antagonist atropine (50 microg/kg), the alpha-adrenergic receptor antagonist phentolamine (200 microg/kg), the beta-adrenergic receptor antagonist propranolol (100 microg/kg), the anti-motilin serum. RESULTS: After motilin was injected into the amygdaloid nucleus, the duodenal MMC cycle duration was decreased significantly, (586.3 +/- 42.0) vs. (694.0 +/- 36.2)s. However, the amplitude of phase III and the frequency of phase III was increased, (294.7 +/- 43.2) vs (255.1 +/- 23.5) microV and (23.1 +/- 0.6) vs. (18.2 +/- 0.4) bursts/min. But there were no effects on the duration of phase III. The percentage change in frequency of phase III was much greater than the percentage change in amplitude of phase III, (54.3 +/- 5.6) vs. (22.4 +/- 4.3). The effects of motilin in the amygdaloid nucleus on MMC were completely abolished by subdiaphragmatic vagotomy. The effects of motilin in the amygdaloid nucleus on MMC were not affected by intravenously injected atropine, phentolamine or propranolol. The anti-motilin serum partly abolished the effects of motilin in the amygdaloid nucleus on MMC. CONCLUSION: Motilin in the amygdaloid nucleus has effects on the duodenal MMC cycle duration, the amplitude of phase III and the frequency of phase III, all of which may rely on either the effects of noncholinergic and nonadrenergic neurons on duodenal smooth muscle, or the increase of local motilin via nucleus amygdalae-hypothalamus-brain stem-vagus pathway.

Amygdala↗
PubMed1977

Migrating myoelectrical complex of the small intestine. An intrinsic activity mediated by the vagus.

In healthy conscious parenterally fed dogs and in sheep on their usual diet, the basic motor profile on the small intestine consists of recurring cycles of action potential activity. This cyclic pattern called the migrating myoelectrical complex comprises two distinct phases termed irregular, and regular spiking activity and is followed by a period of quiescence. The pattern persists after bilateral transthoracic vagotomy and in animals rendered diabetic by alloxan. In dogs, feeding disrupts the migrating myoelectrical complex pattern by obliterating the phases of regular spiking activity and quiescence for 6 to 12 hr, depending upon the amount of dry matter intake. After vagotomy a latency in the disruption of the migrating myoelectrical complex pattern with feeding occurs and in vagotomized dogs rendered diabetic, the duration of disruption is strongly reduced. In sheep, the duration of irregular spiking activity of a jejunal segment increased or decreased corresponding to the bulk of digesta, a phenomenon damped after vagotomy. The results indicate that the role of the vagus is limited to (1) prompting prandial disruption, which is then maintained by hormonal effect; (2) regulating the irregular spiking activity duration in relation to the bulk of digesta.

Action Potentials↗
PubMed1994

Plasma secretin fluctuates in phase with periodic pancreatic secretion and the duodenal migrating myoelectric complex in calves.

Plasma secretin and cholecystokinin (CCK) levels and the periodic secretions of the exocrine pancreas were studied simultaneously with the duodenal migrating myoelectric complexes (MMC) in six milk-fed calves which had been starved overnight. The experiments were performed first when the calves were 10 to 16 days old and subsequently when they were 36 to 45 days old. Plasma secretin and the secretion of pancreatic juice fluctuated periodically in phase with the duodenal MMC: plasma secretin, and the pancreatic secretion of water and protein were significantly higher during the phase of irregular spiking activity than during the phase of no spiking activity in both investigations. Plasma CCK did not change throughout the MMC. The intravenous infusion of secretin at 120 pmol kg-1 bodyweight for one hour markedly stimulated pancreatic secretion and prolonged the duodenal MMC cycle, but it did not abolish pancreatic and duodenal periodic activity.

Aging↗
PubMed1993

Dihydropyridine calcium channel antagonists disrupt migrating myoelectric complexes and counteract intestinal disorders associated with morphine withdrawal diarrhea.

The effects of two dihydropyridine (DHP) calcium channel antagonists, nifedipine and nimodipine, on migrating myoelectric complexes (MMCs) of the small intestine were studied in naive and morphine-dependent rats. In addition, the effects of two other calcium channel antagonists, verapamil and diltiazem, on the MMCs were investigated. Nifedipine (1.0-4.0 mg kg-1 intravenously) or nimodipine (1.0-4.0 mg kg-1 intravenously) had an inhibitory effect on the spontaneously occurring MMCs, whereas verapamil (2.5-5.0 mg kg-1 intravenously) or diltiazem (2.5-5.0 mg kg-1 intravenously) had no effect. Bay K 8644 (0.25 mg kg-1 intravenously), a DHP calcium channel agonist, instantly reversed the inhibition induced by nifedipine or nimodipine. When given alone, Bay K 8644 induced irregular spiking activity. In morphine-dependent rats with regular MMCs naloxone (1.0 mg kg-1 intravenously) induced intense spiking activity and profuse diarrhea. Nifedipine (2.0 and 4.0 mg kg-1 intravenously) and nimodipine (2.0 and 4.0 mg kg-1 intravenously) given before naloxone prevented the intense, abstinence-evoked spiking and associated diarrhea. In healthy volunteers nimodipine at an infusion rate of 2 mg h-1 for 4 h did not inhibit the fasting motility pattern. Our findings indicate that DHP-binding sites are involved in the regulation of MMC in the rat and that drugs acting as antagonists at these sites can be used to suppress morphine withdrawal diarrhea and, tentatively, other functional disorders of the intestine.

Adult↗