Circumferential, not longitudinal, colonic stretch increases synaptic input to mouse prevertebral ganglion neurons

2003 ◽  
Vol 285 (6) ◽  
pp. G1129-G1138 ◽  
Author(s):  
Steven M. Miller ◽  
J. H. Szurszewski
Keyword(s):  
Synaptic Input ◽  
Muscle Tension ◽  
Circular Muscle ◽  
Longitudinal Axis ◽  
Muscle Layer ◽  
Intraluminal Pressure ◽  
Colon Wall ◽  
Mesenteric Ganglion ◽  
Ganglion Neurons

The relationship between longitudinal and circular muscle tension in the mouse colon and mechanosensory excitatory synaptic input to neurons in the superior mesenteric ganglion (SMG) was investigated in vitro. Electrical activity was recorded intracellularly from SMG neurons, and muscle tension was simultaneously monitored in the longitudinal, circumferential, or both axes. Colonic intraluminal pressure and volume changes were also monitored simultaneously with muscle tension changes. The results showed that the frequency of fast excitatory postsynaptic potentials (fEPSPs) in SMG neurons increased when colonic muscle tension decreased, when the colon relaxed and refilled with fluid after contraction, and during receptive relaxation preceding spontaneous colonic contractions. In contrast, fEPSP frequency decreased when colonic muscle tension increased during spontaneous colonic contraction and emptying. Manual stretch of the colon wall to 10-15% beyond resting length in the circumferential axis of flat sheet preparations increased fEPSP frequency in SMG neurons, but stretch in the longitudinal axis to 15% beyond resting length in the same preparations did not. There was no increase in synaptic input when tubular colon segments were stretched in their long axes up to 20% beyond their resting length. The circumferential stretch-sensitive increase in the frequency of synaptic input to SMG neurons persisted when the colonic muscles were relaxed pharmacologically by nifedipine (2 μM) or nicardipine (3 μM). These results suggest that colonic mechanosensory afferent nerves projecting to the SMG function as length or stretch detectors in parallel to the circular muscle layer.

Volume-sensitive synaptic input to neurons in guinea pig inferior mesenteric ganglion

1990 ◽  
Vol 259 (3) ◽  
pp. G490-G497 ◽  
Author(s):  
T. L. Anthony ◽  
D. L. Kreulen
Keyword(s):  
Guinea Pig ◽  
Synaptic Input ◽  
Intraluminal Pressure ◽  
Postsynaptic Potentials ◽  
Inferior Mesenteric Ganglion ◽  
Synaptic Potentials ◽  
Mesenteric Ganglion ◽  
Excitatory Synaptic Input ◽  
The Relationship

The relationship between changes in intracolonic volume related to propulsive contractions and synaptic potentials recorded intracellularly in neurons in the inferior mesenteric ganglion (IMG) was investigated in vitro. Distension of the colon induced propulsive contractions (frequency, 2-5/min), which reduced intracolonic volume by 88%. Each propulsive contraction was sustained for 10-12 s, after which time the colon refilled. The sustained propulsive contractions were associated with a decrease in the amplitude and frequency of fast cholinergic excitatory postsynaptic potentials (EPSPs) and partial repolarization of the slow EPSP. The pressure-volume relationships of the colonic segments had two limbs: at distension pressures less than 15 cmH2O ("volume limb") the intracolonic volume was proportional to the distension pressure; greater than 15 cmH2O ("pressure limb") the intracolonic volume did not increase further. The changes in synaptic input were related to these pressure-volume relationships. In the volume limb, the frequency and amplitude of fast EPSPs were proportional to intracolonic volume and maximized with volume. In the pressure limb, there was a slow depolarization of the membrane that increased with greater distension pressures. Under isovolumic conditions, the changes in intraluminal pressure associated with colonic contractions were not associated with changes in excitatory synaptic input to IMG neurons. These experiments demonstrate that colonic mechanoreceptors to IMG neurons are sensitive to both intracolonic volume and pressure.

Effect of enkephalins on colonic mechanoreceptor synaptic input to inferior mesenteric ganglion

1987 ◽  
Vol 252 (1) ◽  
pp. G128-G135 ◽  
Author(s):  
H. D. Shu ◽  
J. A. Love ◽  
J. H. Szurszewski
Keyword(s):  
Synaptic Input ◽  
Action Potentials ◽  
Input Resistance ◽  
Inhibitory Neurons ◽  
Intraluminal Pressure ◽  
Resting Membrane Potential ◽  
Inferior Mesenteric Ganglion ◽  
Mesenteric Ganglion ◽  
In Vitro Superfusion

The effects of leucine-enkephalin (Leu-Enk) on colonic mechanoreceptor input to the inferior mesenteric ganglion (IMG) and on colonic intraluminal pressure of the guinea pig were studied in vitro. Superfusion of the IMG with Leu-Enk decreased colonic, afferent mechanoreceptor synaptic input. In neurons in which mechanoreceptor input caused postsynaptic spikes, Leu-Enk decreased synaptic input and increased the basal intraluminal pressure of the colon. When mechanoreceptor input consisted of singly occurring excitatory postsynaptic potentials (EPSPs), Leu-Enk decreased the frequency of EPSPs but did not cause a change in colonic pressure. The inhibitory effects of Leu-Enk on synaptic transmission were antagonized by naloxone. In the isolated IMG, Leu-Enk converted synchronous action potentials in response to electrical stimulation of intermesenteric nerves to subthreshold EPSPs without a change in the resting membrane potential or input resistance. Action potentials elicited by depolarizing current pulses or by exogenous acetylcholine were unaltered by Leu-Enk. These data suggest that Leu-Enk increased colonic intraluminal pressure by acting on the presynaptic terminals of colonic mechanoreceptive neurons to reduce synaptic input to and output from the inhibitory neurons of the IMG.

HCl-induced inflammatory mediators in cat esophageal mucosa and inflammatory mediators in esophageal circular muscle in an in vitro model of esophagitis

2006 ◽  
Vol 290 (6) ◽  
pp. G1307-G1317 ◽  
Author(s):  
Ling Cheng ◽  
Weibiao Cao ◽  
Claudio Fiocchi ◽  
Jose Behar ◽  
Piero Biancani ◽  
...  
Keyword(s):  
Inflammatory Mediators ◽  
Platelet Activating Factor ◽  
Circular Muscle ◽  
Muscle Layer ◽  
Normal Mucosa ◽  
Esophageal Mucosa ◽  
Mrna Levels ◽  
Physiol Gastrointest Liver ◽  
Krebs Buffer

Platelet-activating factor (PAF) and interleukin-6 (IL-6) are produced in the esophagus in response to HCl and affect ACh release, causing changes in esophageal motor function similar to esophagitis (Cheng L, Cao W, Fiocchi C, Behar J, Biancani P, and Harnett KM. Am J Physiol Gastrointest Liver Physiol 289: G418–G428, 2005). We therefore examined HCl-activated mechanisms for production of PAF and IL-6 in cat esophageal mucosa and circular muscle. A segment of normal mucosa was tied at both ends, forming a mucosal sac (Cheng L, Cao W, Fiocchi C, Behar J, Biancani P, and Harnett KM. Am J Physiol Gastrointest Liver Physiol 289: G860–G869, 2005) that was filled with acidic Krebs buffer (pH 5.8) or normal Krebs buffer (pH 7.0) as control and kept in oxygenated Krebs buffer for 3 h. The supernatant of the acidic sac (MS-HCl) abolished contraction of normal muscle strips in response to electric field stimulation. The inhibition was reversed by the PAF antagonist CV3988 and by IL-6 antibodies. PAF and IL-6 levels in MS-HCl and mucosa were significantly elevated over control. IL-6 levels in mucosa and supernatant were reduced by CV3988, suggesting that formation of IL-6 depends on PAF. PAF-receptor mRNA levels were not detected by RT-PCR in normal mucosa, but were significantly elevated after exposure to HCl, indicating that HCl causes production of PAF and expression of PAF receptors in esophageal mucosa and that PAF causes production of IL-6. PAF and IL-6, produced in the mucosa, are released to affect the circular muscle layer. In the circular muscle, PAF causes production of additional IL-6 that activates NADPH oxidase to induce production of H2O2. H2O2 causes formation of IL-1β that may induce production of PAF in the muscle, possibly closing a self-sustaining cycle of production of inflammatory mediators.

Origin of Motion in the Human Ureter: Mechanics, Energetics and Kinetics of the Myosin Molecular Motors

2012 ◽  
Vol 79 (2) ◽  
pp. 123-129 ◽  
Author(s):  
Romina Vargiu ◽  
Anna Perinu ◽  
Antonello De Lisa ◽  
Frank Tintrup ◽  
Francesco Manca ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Molecular Motors ◽  
Circular Muscle ◽  
Muscle Layer ◽  
Shortening Velocity ◽  
Smooth Muscle Layer ◽  
Circular Smooth Muscle ◽  
Longitudinal Smooth Muscle ◽  
Human Ureter

Background Ureteral peristalsis is the result of coordinated mechanical motor performance of longitudinal and circular smooth muscle layer of the ureter wall. The main aim of this study was to characterize in smooth muscle of proximal segments of human ureter, the mechanical properties at level of muscle tissue and at level of myosin molecular motors. Methods Ureteral samples were collected from 15 patients, who underwent nephrectomy for renal cancer. Smooth muscle strips longitudinally and circularly oriented from proximal segments of human ureter were used for the in vitro experiments. Mechanical indices including the maximum unloaded shortening velocity (Vmax), and the maximum isometric tension (P0) normalized per cross-sectional area, were determined in vitro determined in electrically evoked contractions of longitudinal and circular smooth muscle strips. Myosin cross-bridge (CB) number per mm2 (Ψ) the elementary force per single CB (Ψ) and kinetic parameters were calculated in muscle strips, using Huxley's equations adapted to nonsarcomeric muscles. Results Longitudinal smooth muscle strips exhibited a significantly (p<0.05) faster Vmax (63%) and a higher P0 (40%), if compared to circular strips. Moreover, longitudinal muscle strips showed a significantly higher unitary force (Ψ) per CB. However, no significant differences were observed in CB number, the attachment (f1) and the detachment (g2) rate constants between longitudinal and circular muscle strips. Conclusions The main result obtained in the present work documents that the mechanical, energetic and unitary forces per CB of longitudinal layer of proximal ureter are better compared to the circular one; these preliminary findings suggested, unlike intestinal smooth muscle, a major role of longitudinal smooth muscle layer in the ureter peristalsis.

Longitudinal contractions in the duodenum: their fluid-mechanical function

1975 ◽  
Vol 228 (6) ◽  
pp. 1887-1892 ◽  
Author(s):  
J Melville ◽  
E Macagno ◽  
J Christensen
Keyword(s):  
Longitudinal Muscle ◽  
Circular Muscle ◽  
Muscle Layer ◽  
Slow Waves ◽  
Longitudinal Muscle Layer ◽  
Circular Muscle Layer ◽  
Model Flow ◽  
Displacement Wave ◽  
Marked Points

The hypothesis examined was that contractions of the longitudinal muscle layer occurin the duodenum which are independent of those of the circular muscle layer and that they induce flow of duodenal contents. A segment of opossum duodenum isolated in vitro was marked and photographed during periods of longitudinal muscle contraction, when the circular muscle layer appeared inactive. The prequency of longitudinal oscillation of the marked points was 20.5 cycles/min. The longitudinal displacement wave spread caudad with an average velocity of 3.27 cm/s. Frequency and velocity of electrical slow waves were determined in similiar duodenal segments. Slow-wave frquencywas 18.9 cycles/min. In a two-dimensional mechanical model, flow induced by simulatedlongitudinal muscle layer appear to be driven by the electrical slow waves of the duodenum. They are capable of inducing a pattern of flow in which ocntents flow betweenthe core and the periphery of the intestinal conduit.

Pylorectomy reduces the satiety action of cholecystokinin

1988 ◽  
Vol 255 (6) ◽  
pp. R1059-R1063 ◽  
Author(s):  
T. H. Moran ◽  
L. Shnayder ◽  
A. M. Hostetler ◽  
P. R. McHugh
Keyword(s):  
Binding Sites ◽  
Contractile Response ◽  
Behavioral Responses ◽  
Circular Muscle ◽  
Muscle Layer ◽  
Pyloric Sphincter ◽  
Cck Receptors ◽  
Physiological Assessment ◽  
Significant Attenuation

Rat gastric cholecystokinin (CCK) receptors are localized to the circular muscle layer of the pyloric sphincter, and a role for these receptors in the mediation of CCK satiety has been proposed. To directly assess the contribution of this receptor population in CCK satiety, the area of the pyloric sphincter containing these receptors was surgically removed, and the behavioral responses to CCK were compared pre- and postpylorectomy. The presence of CCK receptors in the gastroduodenal junction was assessed by either in vitro CCK receptor autoradiography or in vitro contractile response to CCK. The results depended on the time after pylorectomy during which testing occurred. Two to 3 wk after pylorectomy rats demonstrated a significant attenuation of CCK satiety such that while the response to 1 and 2 micrograms/kg was intact, any additional inhibition by 4 and 8 micrograms/kg was eliminated. At this time, no evidence of CCK receptors around the gastroduodenal junction was found. In contrast, 2-3 mo after pylorectomy, the normal dose-response inhibition to CCK was intact. Evidence for the presence of CCK binding sites at the gastroduodenal junction was found by both autoradiography and physiological assessment. These results indicate a role for pyloric CCK receptors in the mediation of CCK satiety.

In vitro model of acute esophagitis in the cat

2005 ◽  
Vol 289 (5) ◽  
pp. G860-G869 ◽  
Author(s):  
Ling Cheng ◽  
Weibiao Cao ◽  
Claudio Fiocchi ◽  
Jose Behar ◽  
Piero Biancani ◽  
...  
Keyword(s):  
In Vitro Model ◽  
Circular Muscle ◽  
Muscle Layer ◽  
Normal Mucosa ◽  
Esophageal Mucosa ◽  
Acute Esophagitis ◽  
Vitro Model ◽  
Esophageal Contraction

We have shown that IL-1β and IL-6, possibly originating from the mucosa in response to injury, inhibit neurally mediated contraction of esophageal circular muscle but do not affect ACh-induced contraction, reproducing the effect of experimental esophagitis on esophageal contraction. To examine the interaction of mucosa and circular muscle in inflammation, we examined the effect of HCl on in vitro esophageal mucosa and circular muscle. Circular muscle strips, when directly exposed to HCl, contracted normally. However, when circular muscle strips were exposed to supernatants of mucosa incubated in HCl (2–3 h, pH 5.8), contraction decreased, and the inhibition was partially reversed by an IL-6 antibody. Supernatants from the mucosa of animals with in vivo-induced acute esophagitis (AE) similarly reduced contraction. IL-6 levels were higher in mucosal tissue from AE animals than in control mucosa and in AE mucosa supernatants than in normal mucosa supernatants. IL-6 levels increased significantly in normal mucosa and supernatants in response to HCl, suggesting increased production and release of IL-6 by the mucosa. IL-6 increased H2O2 levels in the circular muscle layer but not in mucosa. Exposure of the mucosa to HCl caused IL-1β to increase only in the mucosa and not in the supernatant. These data suggest that HCl-induced damage occurs first in the mucosa, leading to the production of IL-1β and IL-6 but not H2O2. IL-1β appears to remain in the mucosa. In contrast, IL-6 is produced and released by the mucosa, eventually resulting in the production of H2O2 by the circular muscle, with this affecting circular muscle contraction.

Influence of intrinsic nerves on electromyogram of cat colon in vitro.

1978 ◽  
Vol 234 (6) ◽  
pp. E641 ◽  
Author(s):  
J Christensen ◽  
S Anuras ◽  
C Arthur
Keyword(s):  
Local Anesthetic ◽  
Circular Muscle ◽  
Muscle Layer ◽  
Slow Waves ◽  
Adrenergic Agonists ◽  
Spike Burst ◽  
Intrinsic Nerves ◽  
Alpha Antagonist ◽  
Spike Bursts

The electromyogram of the circular muscle layer of the cat colon was studied in vitro in superfused strips of muscle. Records exhibited electrical slow waves and migrating spike bursts, as described previously. Both the neurotoxin, tetrodotoxin, and the local anesthetic lidocaine, (P less than 0.05) prolonged the duration of migrating spike bursts, but migrating spike bursts were not affected by the adrenergic alpha-antagonist, phenoxybenzamine, nor by the adrenergic beta-antagonist, propranolol. Also, physostigmine and atropine did not affect them. Large concentrations of catecholamines did abolish them. This suggests that the migrating spike burst represents periodic release of the muscle from the tonic influence of nonadrenergic inhibitory nerves in the intramural plexuses. Slow-wave frequency and the congruence of slow waves were not affected (P greater than 0.05) by the antagonists listed above, nor by cholinergic and adrenergic agonists. This suggests that the slow waves are not importantly controlled by intrinsic nerves.

An electrophysiological study of inferior mesenteric ganglion of the dog

1984 ◽  
Vol 51 (4) ◽  
pp. 607-615 ◽  
Author(s):  
B. F. King ◽  
J. H. Szurszewski
Keyword(s):  
Electrical Activity ◽  
Synaptic Input ◽  
Ganglion Cells ◽  
Sympathetic Neurons ◽  
Electrophysiological Study ◽  
Repetitive Firing ◽  
Resting Membrane Potential ◽  
Inferior Mesenteric Ganglion ◽  
Mesenteric Ganglion

Intracellular recordings were made in vitro from 430 sympathetic neurons in the inferior mesenteric ganglion (IMG) of the dog. Ganglion cells had resting membrane potentials between -35 and -70 mV; input resistance (Rin) was approximately 22 M omega. Cell rheobase to depolarizing current was 0.3 nA, and the action potential elicited was 80-100 mV in amplitude followed by an afterhyperpolarization of up to 15 mV in size, which decayed to the resting membrane potential over a range of 50-500 ms. Neurons were classified as either phasic (188 of 280) or tonic (92 of 280) firing cells, depending on their discharge pattern in response to depolarizing current. Two hundred eight of 430 neurons showed continuous electrical activity in the form of spontaneous excitatory postsynaptic potentials, 2-5 mV in amplitude. Continuous electrical activity was unaffected by tetrodotoxin (3 X 10(-6) M) but abolished by hexamethonium (10(-4) M). A small number of cells (21 of 430) adopted a repetitive firing pattern not associated with injury discharge. These cells may have been pacemaking neurons. Stimulation of peripheral and central nerves resulted in multiple synaptic input to ganglion cells. There was marked convergence of excitatory fibers to any one cell. Evoked synaptic potentials were abolished by hexamethonium (10(-4) M). Synaptic input from peripheral and central nerves could not be correlated with location of postganglionic neurons in the IMG. The possibility of neuronal intercommunication and dissemination of central and peripheral commands is discussed.

Motor controls of opaline secretion in Aplysia californica

1980 ◽  
Vol 43 (3) ◽  
pp. 581-594 ◽  
Author(s):  
S. H. Tritt ◽  
J. H. Byrne
Keyword(s):  
Motor Neurons ◽  
Synaptic Input ◽  
Spike Activity ◽  
Aplysia Californica ◽  
Low Frequency ◽  
Synaptic Activity ◽  
Biophysical Properties ◽  
Ganglion Neurons ◽  
Pleural Ganglion

1. Using combined morphological and electrophysiological techniques, we have identified motor neurons in the right pleural ganglion of Aplysia californica that contribute to the release of opaline from the opaline gland. 2. Three pleural ganglion neurons were found to meet the requirements for identification as opaline gland motor neurons by a) sending processes in nerve P5, which innervates the gland; b) producing contractions of the gland in the absence of central synaptic activity; and c) producing excitatory junctional potentials (EJPs) in cells making up the opaline gland itself. The neurons can be reliably located and have been designated PLR1, PLR2, and PLR3. 3. When gland contraction is measured by the change in luminal pressure, the gland response is a graded function of low-frequency spike activity in the motor neurons. 4. Presumptive EJPs recorded from opaline gland cells are reversibly decreased in size by high extracellular Mg2+ and reversibly increased in size by raising the concentration of extracellular Ca2+. These results suggest that the presumptive EJPs are chemically mediated. The presumptive EJPs show facilitation and posttetanic potentiation. 5. The identified opaline motor neurons may constitute a significant portion of the motor input to the opaline gland via nerve P5 since hyperpolarization of the cells prevents the opaline gland response elicited by right connective stimulation in vitro. 6. We have compared the properties of the opaline motor neurons with the previously identified properties of the ink motor neurons (6--9, 19). Like the ink motor neurons, the opaline motor neurons have high resting potentials, are electrically coupled, and have no spontaneous spike activity. They also receive a slow and long-lasting evoked depolarizing synaptic input, which appears to be mediated by a decreased conductance mechanism. The firing pattern of the opaline motor neurons produced by synaptic input shows the same delayed bursting pattern previously described for the ink motor neurons. 7. The biophysical properties and synaptic input to the ink motor neurons have been shown to affect the features of inking behavior (4, 6--9, 19). The opaline motor neurons share some of these biophysical characteristics and mediate a defensive behavior similar to ink release. Further comparisons of these behaviors and their underlying neural circuits may provide a better understanding of the extent to which cellular biophysical properties and patterns of synaptic input influence the features of the behaviors that individual neurons mediate.

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