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M Schemann

Publications and source records attributed to M Schemann.

At least 91 records · Page 5Linked to original sources
PubMed1993

Actions of nitric oxide-generating sodium nitroprusside in myenteric plexus of guinea pig small intestine.

Sodium nitroprusside (NaNP) was used as a donor of nitric oxide (NO) to investigate actions of NO on electrical and synaptic behavior of single myenteric neurons in guinea pig small intestine. NaNP (10 microM-1 mM) did not affect resting membrane properties of the neurons, except for an occasional decrease in input resistance and hyperpolarization attributable to suppression of excitatory transmitter release. NaNP did not alter fast nicotinic neurotransmission but suppressed noncholinergic slow excitatory postsynaptic potentials (slow EPSPs) in a concentration-dependent manner. Pretreatment with either methylene blue or oxyhemoglobin reduced the inhibitory action of NaNP on the slow EPSPs. Slow EPSP-like responses to microejected substance P or 5-hydroxytryptamine were unaffected by NaNP. The nitric oxide synthase inhibitor, N omega-nitro-L-arginine methyl ester, did not affect resting membrane excitability or excitatory synaptic events in any of the myenteric neurons. The results suggest that NO may not be released extensively as a neurotransmitter at synapses within the myenteric plexus. If myenteric neurons are exposed to NO released from nonneural sources, then the principal action is expected to be presynaptic inhibition of slow synaptic excitation.

Animals↗
PubMed1993

Rhein stimulates electrogenic chloride secretion by activation of submucosal neurons in guinea pig colon.

Conventional flux chamber methods were applied to investigate the mode of action of rhein, an active metabolite derived from colonic microbial fermentation of the naturally occurring sennoside laxatives, in muscle-stripped segments of guinea pig colon. Mucosal or serosal application of rhein (10 nmol/1 to 0.5 mmol/l) resulted in a dose-dependent increase in short-circuit current (Isc) that was superimposed by irregular fluctuations in Isc. The response to electrical field stimulation was increased. The rhein-evoked increase in Isc was reduced by serosal addition of 50 mumol/l bumetanide, 1 mumol/l tetrodotoxin, 1 mumol/l atropine and 10 mumol/l piroxicam but not 100 mumol/l hexamethonium, 1 mumol/l ICS 205 930 or 10 mumol/l cimetidine. The study suggests that rhein activates chloride secretion by excitation of submucosal neurons and release of acetylcholine and endogenous prostaglandins, but not by release of histamine or serotonin.

Acetylcholine↗
PubMed1992

Alpha-adrenoreceptor modulation of neurally evoked circular muscle responses of the guinea pig stomach.

The effects of alpha-adrenergic agonists on transmural-evoked motor responses were investigated in guinea pig gastric corpus in vitro, using preparations stripped of mucosa and orientated to record changes in circular muscle tension. Three tetrodotoxin-sensitive components to a 10 s burst of transmural stimulation could be distinguished: an initial 'on' contraction, an 'off' contraction and a transient relaxation. The 'on' response was blocked by atropine (0.1 microM), while the 'off' response and relaxation were unaffected at this dose. A submaximal dose of acetylcholine was used to assess the sensitivity of the preparation. The alpha 1 agonist L-phenylephrine decreased the amplitude of the 'off' response while simultaneously increasing both the 'on' response and the relaxation, although the response to acetylcholine was unchanged. These effects were dose-dependent and reversed by pretreatment with prazosin. In marked contrast, the alpha 2 agonist clonidine inhibited the 'on' response in a dose-dependent manner without affecting the 'off' response, the relaxation or the response to acetylcholine. Yohimbine reversed the effect of clonidine. We conclude that the inhibitory action of alpha-agonists involves both cholinergic and non-cholinergic pathways, with alpha 1 and alpha 2 adrenoceptors modulating different circuits within the enteric nervous system.

Animals↗
PubMed1992

Presynaptic inhibitory effects of the peptides NPY, PYY and PP on nicotinic EPSPs in guinea-pig gastric myenteric neurones.

1. Neuropeptide Y (NPY), peptide YY (PYY) and pancreatic polypeptide (PP) affect gastrointestinal effector systems. Although their precise mode of action is unknown it is suggested that their effects are partly mediated by enteric neurones. Therefore, the aim of this study was to investigate the effects of NPY, PYY, avian PP (aPP) and bovine PP (bPP) on the electrophysiological behaviour of gastric myenteric neurones using intracellular recording methods. 2. In all thirty-one neurones tested, electrical stimulation of interganglionic fibre tracts evoked cholinergic, nicotinic fast excitatory postsynaptic potentials (fEPSPs). NPY, PYY and bPP (10-500 nM) inhibited the fEPSPs in a concentration-dependent manner. Additionally, these peptides reversibly abolished spontaneously occurring nicotinic fEPSPs. None of the peptides exhibited any effect on the response to exogenously applied acetylcholine or on the postsynaptic excitability of the neurones. The inhibitory effects on the fEPSPs could not be reversed by perfusion of the alpha-adrenoceptor antagonist, phentolamine (1 microM). 3. In contrast, aPP had no significant effect on fEPSPs even when perfused at the high concentration of 1 microM. 4. The results suggest that NPY, PYY and bPP, but not aPP, act presynaptically to inhibit acetylcholine release from myenteric neurones of the gastric corpus, thereby suppressing fEPSPs. The study indicates a modulatory role for NPY, PYY and bPP in synaptic interactions within the enteric nervous system.

Animals↗
PubMed1992

Electrophysiological identification of vagally innervated enteric neurons in guinea pig stomach.

Myenteric "command neurons" are thought to be the interface between extrinsic and intrinsic controls of gut functions and are thought to be responsible for transmission of vagal impulses to enteric microcircuits. To identify, electrophysiologically, myenteric neurons responding to electrical stimulation of the vagus, we developed an in vitro preparation of the gastric myenteric plexus in which the vagal innervation was preserved. The majority of myenteric neurons [102 of 155 (66%)] received fast excitatory postsynaptic potentials (fEPSPs) after stimulation of the vagus. The proportion of neurons receiving vagal input was highest at the lesser curve (98%) and decreased gradually when recordings were made from neurons located toward the greater curve. Only a small proportion of neurons (4 of 85 cells) showed a slow EPSP after a burst of vagal stimulation. No postsynaptic inhibitory potentials were observed. There was no preferential vagal input to either gastric I, gastric II, or gastric III neurons. The fEPSPs were due to the release of acetylcholine acting postsynaptically on nicotinic receptors. The behavior of the fEPSPs suggests multiple vagal inputs to a majority of myenteric neurons. Our observations call into question the concept of enteric command neurons in favor of a divergent vagal input with widespread modulatory influences over gastric enteric neurotransmission.

Animals↗
PubMed1991

Effects of tachykinins on myenteric neurones of the guinea-pig gastric corpus: involvement of NK-3 receptors.

Responses of gastric myenteric neurones evoked by the mammalian tachykinins substance P (SP), neurokinin A (NKA) and neurokinin B (NKB) were investigated using conventional intracellular recording methods. Application of the tachykinins caused a long lasting depolarization of the membrane potential which was associated with increased spike discharge and augmented excitability of the cells. The responses slowly desensitized. Additionally, cross desensitization occurred between SP, NKA and NKB. Both the NK-1 receptor agonist [Sar9,MetO2(11)]SP and the NK-2 receptor agonist [beta-Ala8]NKA(4-10) had no effect on the electrical properties of the neurones. Only the NK-3 receptor agonist [MePhe7]NKB mimicked the excitatory response observed during SP, NKA and NKB applications. [MePhe7]NKB-induced desensitization abolished the response to SP, NKA and NKB. However, long lasting applications of [Sar9,MetO2(11)]SP or [beta-Ala8]NKA(4-10) had no effect on the SP, NKA or NKB responses. The excitatory effect of SP, NKA and NKB remained unchanged during application of the tachykinin analogues [D-Arg1,D-Trp7,9,Leu11]SP and [Tyr5,D-Trp6,8,9,Arg10]NKA(4-10). The results indicate that SP, NKA and NKB act as excitatory neuromodulators within the enteric nervous system of the stomach. The effects of SP, NKA and NKB appeared to be mediated by activation of NK-3 receptors.

Animals↗
PubMed1991

Excitatory and inhibitory effects of norepinephrine on myenteric neurons of the guinea-pig gastric corpus.

The effects of norepinephrine on the electrical and synaptic behaviour of gastric myenteric neurons were investigated in vitro by using conventional intracellular recording methods. Application of norepinephrine (0.1-10 microM) evoked an excitatory effect in 40% of all cells tested. Excitation consisted of a depolarization of the membrane potential associated with increased spike discharge. Phentolamine or prazosin reversibly abolished and (-)phenylephrine mimicked the excitatory norepinephrine response. Yohimbine and clonidine had no effect. Focal electrical stimulation of interganglionic fibre tracts evoked fast excitatory postsynaptic potentials (fEPSPs) in all neurons. Only a minority of these fEPSPs were blocked by norepinephrine. However, fEPSPs evoked by stimulating presumably extrinsic nerves were always totally blocked by norepinephrine. The inhibitory effect of norepinephrine on fEPSPs could be reversed by phentolamine and yohimbine and mimicked by clonidine. Prazosin and phenylephrine had no effect. Isoproterenol and propranolol modified neither the excitatory nor the inhibitory effects. The results indicate that the excitatory effects of norepinephrine on gastric myenteric neurons are mediated by postsynaptic alpha 1 receptors, whereas the inhibitory effects are mediated by presynaptic alpha 2 receptors, which are located presumably on vagal extrinsic nerves. There was no evidence for beta-receptor-mediated effects in gastric myenteric neurons.

Animals↗
PubMed1990

Propagation velocities and frequencies of contractions along canine small intestine.

This study was performed to clarify in detail the behavior of the propagation velocities and frequencies of contractions along the canine small intestine. In conscious dogs, duodenal, jejunal, and ileal contractions were recorded by multiple, closely spaced strain gauges and analyzed by a computerized method. During both the interdigestive and postprandial states, the propagation velocity increased from the duodenal bulb to the distal duodenum and declined aborally within the jejunum, reaching rather constant values in the ileum. The decrease was steepest in the proximal part of the jejunum. In contrast to the propagation velocities, the contraction frequencies were almost constant in the upper small intestine. In the ileum, the contraction frequencies were markedly lower than in the upper small intestine, indicating that the aboral decrease in frequency occurred in the distal parts of the jejunum. We conclude that both the propagation velocities and the frequencies of contractions decline aborally in a nonlinear fashion. However, the nonlinear patterns of the frequency and the propagation velocity gradients are different.

Animals↗
PubMed1989

Immunocytochemical analysis of potential neurotransmitters present in the myenteric plexus and muscular layers of the corpus of the guinea pig stomach.

Recent electrophysiological studies of neurons of the myenteric plexus of the corpus of the guinea pig stomach have revealed that slow synaptic events are extremely rare. In contrast, they are commonly encountered in similar investigations of myenteric ganglia of the guinea pig small intestine. The current immunocytochemical analysis of the myenteric plexus and innervation of the muscularis externa of the corpus of the guinea pig stomach was undertaken in order to determine whether putative neurotransmitters capable of mediating slow synaptic events are present in gastric ganglia. A major difference between the small intestine and the stomach was found in the innervation of the musculature. Whereas the longitudinal muscle layer of the small intestine contains very few nerve fibers and is innervated mainly at its interface with the myenteric plexus, the longitudinal muscle of the corpus of the stomach contained as many varicose substance P (SP)-, vasocative intestinal polypeptide (VIP)-, and neuropeptide Y (NPY)-immunoreactive axons as the circular muscle layer. These putative neurotransmitters were also present in the ganglia of the myenteric plexus, where varicose SP-, VIP-, and NPY-immunoreactive fibers encircled nonimmunoreactive neurons. Varicose 5-hydroxytryptamine (5-HT)-immunoreactive terminal axons were essentially limited to the myenteric plexus and were found both in ganglia and in interganglionic connectives, where they were particularly numerous; 5-HT-immunoreactive neurons appeared to be more abundant in the stomach than in the small intestine. Tyrosine hydroxylase (TH)- and calcitonin-gene-related-peptide (CGRP)-immunoreactive axons were also more common in the myenteric plexus than in the musculature, but of these, only the TH-immunoreactive neurites tended, like those of the other putative transmitters, to encircle neurons in myenteric ganglia. Evidence was obtained that, as in the small intestine, at least some of the SP-, VIP-, NPY-, and 5-HT-immunoreactive fibers in the stomach are derived from intrinsic gastric myenteric neurons. In contrast, unlike the small intestine, gastric myenteric ganglia appeared to lack intrinsic CGRP-immunoreactive neurons; therefore, the CGRP-immunoreactive gastric axons are probably of extrinsic origin.(ABSTRACT TRUNCATED AT 400 WORDS)

5-Hydroxytryptophan↗
PubMed1989

Electrical behaviour of myenteric neurones in the gastric corpus of the guinea-pig.

1. Electrical behaviour of ganglion cells in the myenteric plexus of the guinea-pig stomach was investigated using intracellular recording methods. 2. Three subpopulations were identified and classified for convenience of discussion as gastric I, II and III neurones. Gastric I neurones were characterized by repetitive spike discharge during depolarizing current pulses and by higher input resistance than the other types. Gastric II neurones discharged one or two spikes only at the onset of long-lasting depolarizing current pulses. Gastric III neurones did not discharge spikes to depolarizing current pulses and had higher membrane potentials and lower input resistances than the other types. Non-stimulus evoked discharge ('spontaneous' discharge) did not occur in any of the neurones. 3. Resting membrane potentials were generated primarily by resting K+ conductance, but were smaller than the estimated K+ equilibrium potential. Analysis based on the constant field equation predicted lower K+ conductance in gastric I than in gastric III neurones. 4. Action potentials in gastric I and II neurones were suppressed or blocked by tetrodotoxin. Spikes that were broadened by tetraethylammonium appeared to have an inward component of Ca2+ current. 5. Hyperpolarizing after-potentials were associated with the spikes of both kinds of neurones. These after-potentials had much shorter duration (less than 300 ms) than the post-spike hyperpolarization of AH/type 2 intestinal neurones and unlike intestinal neurones there was no latency between the positive after-potential of the spike and the onset of the hyperpolarization. After-hyperpolarization in the gastric neurones was enhanced when the spikes were broadened by tetraethylammonium and was suppressed by removal of Ca2+ from the bathing solution. 6. Treatment with either tetraethylammonium or 4-aminopyridine enhanced excitability and induced 'spontaneously' occurring repetitive spike discharge. 7. The electrophysiological behaviour of gastric myenteric neurones differed significantly from intestinal neurones. This was interpreted as specialization of the neural networks that control and co-ordinate the activity of vastly different effector systems in the two regions of the alimentary canal.

Animals↗
PubMed1989

Synaptic behaviour of myenteric neurones in the gastric corpus of the guinea-pig.

1. Synaptic behaviour of ganglion cells in the myenteric plexus of the corpus of the guinea-pig stomach was investigated using intracellular recording methods. Synaptic potentials were evoked by focal electrical stimulation of interganglionic fibre tracts or the surface of the ganglion containing the cell body from which the recording was obtained. 2. Fast excitatory postsynaptic potentials (EPSPs) mediated by nicotinic cholinergic receptors were the most common stimulus-evoked or spontaneously occurring synaptic events. 3. Fast EPSPs were evoked in every neurone and most neurones received multiple inputs from axons arriving in several different interganglionic fibre tracts. Several neurones received input from multiple axons in individual fibre tracts. 4. Fast EPSPs were evoked at stimulus frequencies up to 80 Hz without evidence of the 'run-down' phenomenon that characterizes fast EPSPs in the intestine. 5. Trains of EPSPs in the ganglion cell soma occurred with relatively long latencies following spike discharge evoked by intracellular current injection in the same neurone. This appeared to reflect return of excitatory synaptic input to the soma along recurrent connections within the synaptic network. 6. The safety factor for fast EPSPs to evoke spike discharge was highest for gastric I neurones. Probability of fast EPSPs triggering spikes was intermediate in neurones classified electrophysiologically as gastric II and was lowest in gastric III neurones, which never discharged spikes during a fast EPSP. 7. No slow excitatory or inhibitory synaptic potentials, like those found in intestinal ganglion cells, were evoked in gastric neurones by focal stimulation of the fibre tracts. 8. The results suggest that myenteric neurones in the gastric corpus of the guinea-pig have distinctive synaptic behaviour different from intestinal neurones in the same animal. This may be a reflection of adaptation for neural control of the specialized function of the effector systems in this region of the stomach.

Animals↗
PubMed1987

Gastric emptying after Roux-Y and Billroth-I gastrectomy depends on viscosity of meal and contractile patterns of small intestine in dogs.

The aim of the study was to examine gastrointestinal motility after distal gastrectomy and the influence of meal viscosity on gastric emptying. Gastrointestinal motility and gastric emptying of acaloric meals with different viscosities were measured in normal dogs and after a two-thirds gastrectomy with Billroth-I or Roux-Y gastroenterostomy. After distal gastrectomy, gastric emptying depended on the viscosity of the meal, as in normal dogs. Acaloric viscous meals emptied significantly faster in the Billroth-I than in the Roux-Y group due to different contractile patterns of the duodenum and jejunum. In comparison to normal dogs, gastric emptying of viscous meals was accelerated in the Billroth-I and delayed in the Roux-Y group. Several motility parameters of the stomach and intestine differed between the normal and gastrectomized dogs. Thus, after distal gastrectomy, the viscosity of the meal and the contractile patterns of the small intestine are important determinants of gastric emptying.

Animals↗
PubMed1987

Motor patterns of small intestine determined by closely spaced extraluminal transducers and videofluoroscopy.

In the canine small intestine several simple (S) and complex (C) patterns of propulsive and nonpropulsive activities were found. The nonpropulsive activity consisted of 1) stationary individual contractions (S) and 2) stationary clusters of contractions (C). Patterns leading to aboral propulsion of luminal contents were 1) propagating contractions (S), 2) propagating power contractions (S), 3) phase III of the migrating motor complex (C), and 4) migrating clusters of contractions (C). The propagation velocities of the propulsive motor patterns differed markedly; they increased in the following order: phase III, migrating clustered contractions, propagating power contractions, propagating contractions. A retrograde transport of luminal contents was produced by two different activities: 1) retrograde propagating contractions (S) and 2) retrograde power contractions (S). They were accompanied with enterogastric reflux.

Animals↗
PubMed1986

Calcitonin gene-related peptide excites myenteric neurons.

Intracellular methods were used to record electrical behavior of myenteric neurons in guinea-pig ileum in vitro. Calcitonin gene-related peptide (CGRP; 1 nM to 1 microM) and calcitonin (1-100 microM) were applied by addition to the superfusion solution of longitudinal muscle-myenteric plexus preparations. Both peptides were applied also by pressure ejection from fine-tipped micropipettes. CGRP, applied by either method, evoked a long-lasting depolarization of the cell membranes that was dose-dependent (ED50 = 50 nM) and was associated with an increase in the input resistance, suppression of post-spike hyperpolarizing potentials and enhanced excitability in all neurons that were tested. The enhanced excitability was reflected by a significant increase in the number of action potentials evoked by intracellular injection of constant current depolarizing pulses. Enhanced excitability also was apparent as a train of spikes that appeared at the crests of the CGRP-induced depolarization. The excitatory action of CGRP simulated slow synaptic excitation. Application of calcitonin did not evoke any changes in electrical behavior of myenteric neurons. The results are consistent with a neurotransmitter or neuromodulator role for CGRP in the enteric nervous system and suggest that it may participate in local neurohumoral regulation of gastrointestinal effector systems.

Action Potentials↗
PubMed1986

Effects of neurohormonal agents on jejunal contraction spread and transit in the fed dog.

The jejunal contraction patterns of dogs in response to intravenous infusion of neurotensin, somatostatin, secretin, and met-enkephalin were analyzed. The peptides were given after administration of a noncaloric viscous cellulose meal. A computer was used to determine the length of spread of contraction waves, their contraction force, the contraction frequency, and the motility index. Transit rates of luminal content were assessed videofluoroscopically. During saline infusion the cellulose meal was propelled aborally at a transit rate of 3.1 +/- 1.1 cm/s; the corresponding length of spread of contraction waves was 10.3 +/- 1.5 cm. All peptides decreased both the transit rate (0.45-1.81 cm/s) and the contraction spread (3.7-6.2 cm). Neurotensin increased the contraction force, but had no effect on contraction frequency and motility index. The other peptides reduced the motility index and the frequency and force of contractions. It was shown that the peptides influenced intestinal contraction patterns and the transit rate of luminal content. The length of spread of contraction waves was found to be most important in the regulation of transit.

Animals↗