Generation of spiking activity in circular muscle cells of the canine colon

1987 ◽  
Vol 65 (10) ◽  
pp. 2147-2150 ◽  
Author(s):  
Jan D. Huizinga ◽  
Carlos Barajas-Lopez ◽  
Edwin Chow
Keyword(s):  
Myenteric Plexus ◽  
Contractile Activity ◽  
Extracellular Recording ◽  
Circular Muscle ◽  
Muscle Cells ◽  
Muscle Layer ◽  
Organ Bath ◽  
Force Of Contraction ◽  
Plateau Potential ◽  
Spiking Activity

Spontaneous and current-induced electrical activity was recorded intracellularly to resolve the controversy whether or not the circular muscle layer of the colon generates spiking activity. Particularly in the first hour after mounting the tissue in the organ bath, spikes were recorded at both the submucosal and the myenteric plexus side of the muscle layer. Spikes were seen as part of the slow wave upstroke in the submucosal surface cells, and spikes occurred both at the upstroke potential and superimposed on the plateau potential in myenteric plexus surface cells. Spikes increased the force of contraction. The study supports earlier claims using extracellular recording techniques that circular muscle cells generate spiking activity, particularly in the presence of depolarizing stimuli, and that spikes contribute to contractile activity.

The effects of cholecystokinin-octapeptide and pentagastrin on electrical and motor activities of canine colonic circular muscle

1984 ◽  
Vol 62 (12) ◽  
pp. 1440-1447 ◽  
Author(s):  
Jan D. Huizinga ◽  
Gordon Chang ◽  
Nicholas E. Diamant ◽  
Taher Y. El-Sharkawy
Keyword(s):  
Contractile Activity ◽  
Colonic Motility ◽  
Circular Muscle ◽  
Slow Waves ◽  
Organ Bath ◽  
Experimental Conditions ◽  
Cholecystokinin Octapeptide ◽  
Plateau Potential ◽  
Motor Activities ◽  
Spiking Activity

The effects of cholecystokinin-octapeptide (CCK-OP) and pentagastrin on electrical and motor activities of circular muscle of the canine colon were studied with the sucrose gap technique. Additional organ bath experiments were performed to further characterize the motor response to the peptides and to elucidate their site of action. The electrical activity consisted of slow waves having an initial potential followed by a plateau potential, at a regular frequency of 4.5 cycles/min. Both peptides prolonged the duration and increased the amplitude of the plateau phase of the slow waves. Concomitantly, the slow wave frequency was reduced. In addition, CCK-OP increased spiking activity. Both spiking activity and the prolonged plateau potential generated contractile activity, prolonged phasic contraction occurring with slow waves with a prolonged plateau. In organ bath experiments, both CCK-OP and pentagastrin increased the basal tone of the muscle strips and prolonged the duration of the phasic contractions. The prolongation of the duration of the contractions was not antagonized by tetrodotoxin (TTX) and atropine. CCK-OP but not pentagastrin increased the force of contractions, this action was not affected by atropine but was reduced in the presence of TTX, suggesting that the increase in force may be partially mediated by noncholinergic excitatory nerves. The increase in basal tension by the peptides was enhanced in the presence of TTX indicating that myenteric inhibitory neurones were tonically active under our experimental conditions. The results provide the electrophysiological basis for CCK-OP and pentagastrin induced changes in colonic motility.

Pacemaker potentials generated by interstitial cells of Cajal in the murine intestine

2005 ◽  
Vol 288 (3) ◽  
pp. C710-C720 ◽  
Author(s):  
Yoshihiko Kito ◽  
Sean M. Ward ◽  
Kenton M. Sanders
Keyword(s):  
Interstitial Cells Of Cajal ◽  
Circular Muscle ◽  
Muscle Cells ◽  
Interstitial Cells ◽  
Slow Waves ◽  
Pacemaker Activity ◽  
Dependent Manner ◽  
Plateau Potential ◽  
Pacemaker Potentials ◽  
Cells Of Cajal

Pacemaker potentials were recorded in situ from myenteric interstitial cells of Cajal (ICC-MY) in the murine small intestine. The nature of the two components of pacemaker potentials (upstroke and plateau) were investigated and compared with slow waves recorded from circular muscle cells. Pacemaker potentials and slow waves were not blocked by nifedipine (3 μM). In the presence of nifedipine, mibefradil, a voltage-dependent Ca2+ channel blocker, reduced the amplitude, frequency, and rate of rise of upstroke depolarization (d V/d tmax) of pacemaker potentials and slow waves in a dose-dependent manner (1–30 μM). Mibefradil (30 μM) changed the pattern of pacemaker potentials from rapidly rising, high-frequency events to slowly depolarizing, low-frequency events with considerable membrane noise (unitary potentials) between pacemaker potentials. Caffeine (3 mM) abolished pacemaker potentials in the presence of mibefradil. Pinacidil (10 μM), an ATP-sensitive K+ channel opener, hyperpolarized ICC-MY and increased the amplitude and d V/d tmax without affecting frequency. Pinacidil hyperpolarized smooth muscle cells and attenuated the amplitude and d V/d tmax of slow waves without affecting frequency. The effects of pinacidil were blocked by glibenclamide (10 μM). These data suggest that slow waves are electrotonic potentials driven by pacemaker potentials. The upstroke component of pacemaker potentials is due to activation of dihydropyridine-resistant Ca2+ channels, and this depolarization entrains pacemaker activity to create the plateau potential. The plateau potential may be due to summation of unitary potentials generated by individual or small groups of pacemaker units in ICC-MY. Entrainment of unitary potentials appears to depend on Ca2+ entry during upstroke depolarization.

Substance P and CGRP mediate motor response of rabbit colon to capsaicin

1990 ◽  
Vol 259 (5) ◽  
pp. G889-G897 ◽  
Author(s):  
E. A. Mayer ◽  
C. B. Koelbel ◽  
W. J. Snape ◽  
V. Eysselein ◽  
H. Ennes ◽  
...  
Keyword(s):  
Substance P ◽  
Longitudinal Muscle ◽  
Contractile Activity ◽  
Circular Muscle ◽  
Muscle Layer ◽  
Inhibitory Effect ◽  
Nerve Fibers ◽  
Repeated Exposure ◽  
Nerve Terminals ◽  
Rabbit Colon

Primary afferent nerve terminals located in the mammalian gut wall may play a role in region-specific modulation of gastrointestinal motility. In the present study, we sought to characterize the effect of neuropeptides released from these afferents by capsaicin (CAP) on contractile activity of smooth muscle from the distal rabbit colon. CAP caused a release of acetylcholine and immunoreactivity for substance P (SP) and calcitonin gene-related peptide (CGRP) from the muscle coat. CAP caused a dose-dependent transient stimulation of longitudinal muscle contractions, followed by prolonged inhibition of spontaneous but not stimulated contractile activity. The initial stimulation was abolished by the SP antagonist spantide and by atropine. The inhibitory effect was reduced by repeated exposure of muscle to CGRP. The effect of CGRP on spontaneous contractions differed between longitudinal and circular muscle. In longitudinal muscle, a stimulation was preceded by a transient inhibition, whereas in circular muscle, only inhibition was seen. Both effects were resistant to tetrodotoxin. Repeated exposure of circular but not longitudinal muscle to CGRP resulted in a disappearance of the peptide's inhibitory effect. Exogenously applied CGRP was only a weak antagonist of contractions stimulated by SP and bethanechol. These findings suggest that in the rabbit colon at least the following two neuropeptides are released from CAP-sensitive nerve fibers: a neurokinin peptide from nerve terminals located within the myenteric plexus and CGRP from terminals probably located within the circular muscle layer.

The sacral neural crest contributes neurons and glia to the post-umbilical gut: spatiotemporal analysis of the development of the enteric nervous system

Development ◽  
1998 ◽  
Vol 125 (21) ◽  
pp. 4335-4347 ◽  
Author(s):  
A.J. Burns ◽  
N.M. Le Douarin
Keyword(s):  
Nervous System ◽  
Neural Crest ◽  
Enteric Nervous System ◽  
Myenteric Plexus ◽  
Circular Muscle ◽  
Muscle Layer ◽  
Specific Marker ◽  
Circular Muscle Layer ◽  
Sacral Neural Crest ◽  
Antibody Labelling

The majority of the enteric nervous system is derived from vagal neural crest cells (NCC), which migrate to the developing gut, proliferate, form plexuses and differentiate into neurons and glia. However, for some time, controversy has existed as to whether cells from the sacral region of the neural crest also contribute to the enteric nervous system. The aim of this study was to investigate the spatiotemporal migration of vagal and sacral NCC within the developing gut and to determine whether the sacral neural crest contributes neurons and glia to the ENS. We utilised quail-chick chimeric grafting in conjunction with antibody labelling to identify graft-derived cells, neurons and glia. We found that vagal NCC migrated ventrally within the embryo and accumulated in the caudal branchial arches before entering the pharyngeal region and colonising the entire length of the gut in a proximodistal direction. During migration, vagal crest cells followed different pathways depending on the region of the gut being colonised. In the pre-umbilical intestine, NCC were evenly distributed throughout the splanchnopleural mesenchyme while, in the post-umbilical intestine, they occurred adjacent to the serosal epithelium. Behind this migration front, NCC became organised into the presumptive Auerbach's and Meissner's plexuses situated on either side of the developing circular muscle layer. The colorectum was found to be colonised in a complex manner. Vagal NCC initially migrated within the submucosa, internal to the circular muscle layer, before migrating outwards, adjacent to blood vessels, towards the myenteric plexus region. In contrast, sacral NCC, which also formed the entire nerve of Remak, were primarily located in the presumptive myenteric plexus region and subsequently migrated inwards towards the submucosal ganglia. Although present throughout the post-umbilical gut, sacral NCC were most numerous in the distal colorectum where they constituted up to 17% of enteric neurons, as identified by double antibody labelling using the quail-cell-specific marker, QCPN and the neuron-specific marker, ANNA-1. Sacral NCC were also immunopositive for the glial-specific antibody, GFAP, thus demonstrating that this region of the neural crest contributes neurons and glia to the enteric nervous system.

Selective accumulation of methylene blue by interstitial cells of Cajal in canine colon

1993 ◽  
Vol 264 (1) ◽  
pp. G64-G73 ◽  
Author(s):  
L. W. Liu ◽  
L. Thuneberg ◽  
E. E. Daniel ◽  
J. D. Huizinga
Keyword(s):  
Methylene Blue ◽  
Interstitial Cells Of Cajal ◽  
Three Dimensional ◽  
Circular Muscle ◽  
Muscle Cells ◽  
Muscle Layer ◽  
Interstitial Cells ◽  
Resting Membrane Potential ◽  
Selective Staining ◽  
Cells Of Cajal

The network of interstitial cells of Cajal (ICC) at the submucosal surface of the canine colon was selectively stained by incubation with 15-50 microM methylene blue for 30-45 min. The network was composed of regularly scattered ICC cell bodies interconnected by long processes. Circular muscle cells were unstained. Staining of neurons was limited to one or two axons within bundles. The ICC network had a thickness of a single cell, since no overlapping of ICC cell bodies was observed. The ICC network connected the circular muscle cells at the submucosal surface across the septa which circumferentially divided the circular muscle into lamellae. Methylene blue at 50 microM slightly decreased the resting membrane potential and increased the duration of slow waves, leading to an increase in the force of phasic contractions, with no significant influence on other slow-wave parameters. Methylene blue produced neither electrophysiological nor mechanical effects on circular muscle preparations from which the submuscular ICC network was removed, indicating that the excitatory effects of methylene blue on the full-thickness circular muscle layer were mediated by ICC. In summary, the three-dimensional aspects of the submuscular ICC network can be visualized after selective staining by methylene blue. This staining does not affect physiological characteristics of smooth muscle cells.

LPS-induced muscularis macrophage nitric oxide suppresses rat jejunal circular muscle activity

1999 ◽  
Vol 277 (2) ◽  
pp. G478-G486 ◽  
Author(s):  
Mark K. Eskandari ◽  
Jörg C. Kalff ◽  
Timothy R. Billiar ◽  
Kenneth K. W. Lee ◽  
Anthony J. Bauer
Keyword(s):  
Nitric Oxide ◽  
Muscle Activity ◽  
Contractile Activity ◽  
Circular Muscle ◽  
Fold Increase ◽  
Inos Mrna ◽  
Organ Bath ◽  
Cellular Mechanisms ◽  
Circular Smooth Muscle

Cellular mechanisms of sepsis-induced ileus remain an enigma. The study aim was to determine the role of nitric oxide (NO) in mediating the suppression of rat jejunal circular smooth muscle activity during endotoxemia. Isolated muscularis inducible NO synthase (iNOS) mRNA was measured by RT-PCR, immunohistochemistry was employed to localize iNOS protein, and contractile activity was measured in an organ bath. The low basal expression of muscularis iNOS mRNA expression was increased in a time-dependent fashion after lipopolysaccharide (LPS), resulting in a 20-fold increase over controls 3 h after injection. Immunohistochemistry of muscularis whole mounts and dissociated muscularis cells for iNOS revealed staining only in the muscularis macrophages 12 h after LPS. LPS caused a 68% reduction in spontaneous muscle activity 12 h after injection, which improved by 53% after the in vitro application of the selective iNOS inhibitorl- N6-(1-iminoethyl)lysine. Similar results were obtained in C57BL/6 mice but not in iNOS knockout mice. These data demonstrate that macrophage iNOS plays an important role in mediating LPS-induced intestinal circular muscle suppression.

Electrical slow-wave activity from the circular layer of cat terminal antrum

1991 ◽  
Vol 261 (1) ◽  
pp. G78-G82
Author(s):  
L. M. Renzetti ◽  
M. B. Wang ◽  
J. P. Ryan
Keyword(s):  
Slow Wave ◽  
Circular Muscle ◽  
Muscle Cells ◽  
Muscle Layer ◽  
Wave Activity ◽  
Slow Waves ◽  
Slow Wave Activity ◽  
Plateau Phase ◽  
Circular Layer ◽  
Upstroke Velocity

Intracellular recording techniques were used to characterize the electrical slow-wave activity through the thickness of the circular muscle layer of the cat terminal antrum. Muscle strips were pinned out in cross section to the floor of a recording chamber perfused with Krebs buffer. Circular muscle cells from the myenteric to the submucosal border then were impaled with 20- to 40-M omega glass microelectrodes, and slow-wave activity was recorded. Slow waves from the myenteric side of the circular layer consisted of an upstroke depolarization, a prominent plateau phase, and a downstroke repolarization. Slow-wave characteristics for cells along the myenteric border were Em, -74.2 +/- 1.3 mV; duration, 5.3 +/- 0.5 s; upstroke amplitude, 29.4 +/- 3.4 mV; upstroke velocity, 0.20 +/- 0.03 V/s; and frequency, 5.8 +/- 0.5/min. Slow waves from muscle cells along the submucosal side of the preparation lacked a discernible plateau phase. Slow waves from submucosal border cells had the following characteristics: Em, -80.4 +/- 1.4 mV (P less than 0.01); duration, 3.5 +/- 0.4 s (P less than 0.01); upstroke amplitude, 44.0 +/- 2.4 mV (P less than 0.01); upstroke velocity, 0.56 +/- 0.06 V/s (P less than 0.01); and frequency, 4.2 +/- 0.4/min (P less than 0.05). Slow waves were not affected by 10(-7)M tetrodotoxin and 10(-6)M atropine or by removal of the longitudinal muscle layer. Slow-wave activity within each region was maintained after dissecting the circular layer into submucosal and myenteric segments. The results suggest that two distinct slow waves exist within the circular muscle layer of the cat terminal antrum.(ABSTRACT TRUNCATED AT 250 WORDS)

Primary structure, distribution, and effects on motility of CGRP in the intestine of the cod Gadus morhua

1998 ◽  
Vol 275 (1) ◽  
pp. R19-R28 ◽  
Author(s):  
Fatemeh Shahbazi ◽  
Paul Karila ◽  
Catharina Olsson ◽  
Susanne Holmgren ◽  
J. Michael Conlon ◽  
...  
Keyword(s):  
Amino Acid ◽  
Primary Structure ◽  
Myenteric Plexus ◽  
Gadus Morhua ◽  
Circular Muscle ◽  
Muscle Layer ◽  
Inhibitory Response ◽  
Nerve Fibers ◽  
Amino Acid Substitutions ◽  
Circular Muscle Layer

Calcitonin gene-related peptide (CGRP) was isolated from an extract of the intestine of the cod Gadus morhua. The primary structure of this 37-amino acid peptide was established as follows: ACNTA TCVTH RLADF LSRSG GIGNS NFVPT NVGSK AF-NH2. The peptide shows close structural similarities to other nonmammalian (3–4 amino acid substitutions) and mammalian (5–8 amino acid substitutions) CGRPs, and it contains the two residues Asp14 and Phe15 that seem to be characteristic for CGRP in nonmammalian vertebrates. Cod CGRP (10−9–10−7M) inhibited the motility of spontaneously active ring preparations from the cod intestine and was significantly ( P < 0.05) more potent than rat α-CGRP. Neither prostaglandins nor nitric oxide is involved in the inhibitory response produced by cod CGRP, and the lack of effect of tetrodotoxin suggests an action of CGRP on receptors on the intestinal smooth muscle cells. The competitive CGRP antagonist human α-CGRP-(8—37) significantly ( P < 0.05) reduced the response to cod CGRP. Immunohistochemistry demonstrated CGRP-immunoreactive neurons intrinsic to the intestine, and a dense innervation with immunoreactive nerve fibers was observed in the myenteric plexus and the circular muscle layer. Myotomy studies show that CGRP-containing nerves project orally and anally in the myenteric plexus, whereas nerve fibers in the circular muscle layer project mainly anally, indicating a role for CGRP in descending inhibitory pathways of the cod intestine.

Different mechanisms of contraction generation in circular muscle of canine colon

1989 ◽  
Vol 256 (3) ◽  
pp. G570-G580 ◽  
Author(s):  
C. Barajas-Lopez ◽  
J. D. Huizinga
Keyword(s):  
Slow Wave ◽  
Myenteric Plexus ◽  
Calcium Influx ◽  
Direct Action ◽  
Circular Muscle ◽  
Outward Current ◽  
Muscle Layer ◽  
Circular Muscle Layer ◽  
Mechanical Threshold ◽  
In Cells

Smooth muscle cells from the circular muscle layer of the dog colon showed a mechanical threshold of -44 mV. No gradient in mechanical threshold was measured between the cells from the submucosal and myenteric plexus surface. The threshold was passed during the upstroke and the plateau phase of the spontaneous slow-wave activity from cells at the submucosal surface and by spike potentials occurring mainly in cells at the myenteric plexus surface and sporadically in cells at the submucosal surface. Carbachol-induced specific changes in electrical and mechanical activities that were inhibited by calcium influx blockade are as follows: 1) increase in slow-wave duration; 2) decrease in plateau potential; 3) enhancement of spiking activity; and 4) increase in contractility. This indicates that calcium influx is significantly increased in the presence of carbachol in cells at both surfaces of the circular muscle layer. The increase in calcium influx could be the result of a direct action by carbachol on the calcium conductance and/or could be mediated by a decrease in outward current. The latter is suggested by the carbachol-induced membrane depolarization associated with an increase in the input resistance, which were both methoxyverapamil insensitive. The results show that an excitatory stimulus can generate contraction of the circular muscle through different electrophysiological activities. In addition, the patterns of spontaneous electrical activity and the different responses to carbachol stimulation provide further information about the heterogeneous nature of the electrical activities within the colonic circular muscle layer.

Membrane potential gradient is carbon monoxide-dependent in mouse and human small intestine

2007 ◽  
Vol 293 (2) ◽  
pp. G438-G445 ◽  
Author(s):  
Lei Sha ◽  
Gianrico Farrugia ◽  
W. Scott Harmsen ◽  
Joseph H. Szurszewski
Keyword(s):  
Carbon Monoxide ◽  
Smooth Muscle ◽  
Small Intestine ◽  
Smooth Muscle Cells ◽  
Circular Muscle ◽  
Muscle Cells ◽  
Muscle Layer ◽  
Wild Type ◽  
Circular Smooth Muscle ◽  
Human Small Intestine

The aims of this study were to quantify the change in resting membrane potential (RMP) across the thickness of the circular muscle layer in the mouse and human small intestine and to determine whether the gradient in RMP is dependent on the endogenous production of carbon monoxide (CO). Conventional sharp glass microelectrodes were used to record the RMPs of circular smooth muscle cells at different depths in the human small intestine and in wild-type, HO2-KO, and W/WV mutant mouse small intestine. In the wild-type mouse and human intestine, the RMP of circular smooth muscle cells near the myenteric plexus was −65.3 ± 2 mV and −58.4 ± 2 mV, respectively, and −60.1 ± 2 mV and −49.1 ± 1 mV, respectively, in circular smooth muscle cells at the submucosal border. Oxyhemoglobin (20 μM), a trapping agent for CO, and chromium mesoporphyrin IX, an inhibitor of heme oxygenase, abolished the transwall gradient. The RMP gradients in mouse and human small intestine were not altered by NG-nitro-l-arginine (200 μM). No transwall RMP gradient was found in HO2-KO mice and W/WV mutant mice. TTX (1 μM) and 1H-[1,2,4-]oxadiazolo[4,3-a]quinoxalin-1-one (10 μM) had no effect on the RMP gradient. These data suggest that the gradient in RMP across the thickness of the circular muscle layer of mouse and human small intestine is CO dependent.

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