Electrophysiological identification of vagally innervated enteric neurons in guinea pig stomach

1992 ◽  
Vol 263 (5) ◽  
pp. G709-G718 ◽  
Author(s):  
M. Schemann ◽  
D. Grundy
Keyword(s):  
Nicotinic Receptors ◽  
Vagal Stimulation ◽  
Enteric Neurons ◽  
Command Neurons ◽  
Myenteric Neurons ◽  
Release Of Acetylcholine ◽  
Vagal Innervation ◽  
Guinea Pig Stomach ◽  
Stimulation Of

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.

Vagal regulation of GRP, gastric somatostatin, and gastrin secretion in vitro

1985 ◽  
Vol 248 (4) ◽  
pp. E425-E431 ◽  
Author(s):  
S. Nishi ◽  
Y. Seino ◽  
J. Takemura ◽  
H. Ishida ◽  
M. Seno ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Nicotinic Receptors ◽  
Vagal Stimulation ◽  
Inhibitory Neuron ◽  
Atropine Sulfate ◽  
Vagus Nerves ◽  
Gastrin Secretion ◽  
Somatostatin Secretion ◽  
Stimulation Of

The effect of electrical stimulation of the vagus nerves on the release of immunoreactive gastrin-releasing peptide (GRP), gastrin, and somatostatin was investigated using the isolated perfused rat stomach. Electrical stimulation (10 Hz, 1 ms duration, 10 V) of the peripheral end of the subdiaphragmatic vagal trunks produced a significant increase in both GRP and gastrin but a decrease in somatostatin. The infusion of atropine sulfate at a concentration of 10(-5) M augmented GRP release and reversed the decrease in somatostatin release in response to vagal stimulation to an increase above basal levels. However, the gastrin response to vagal stimulation was not affected by atropine. The infusion of hexamethonium bromide at a concentration of 10(-4) M significantly suppressed GRP release but did not affect gastrin secretion in response to vagal stimulation. On the other hand, the somatostatin response to vagal stimulation was completely abolished by hexamethonium. These findings lead us to conclude that the intramural GRP neurons might play an important role in the regulation of gastrin as well as somatostatin secretion and that somatostatin secretion may be controlled not only by a cholinergic inhibitory neuron but also by a noncholinergic, e.g., peptidergic stimulatory neuron, both of which may be regulated through preganglionic vagal fibers via nicotinic receptors. In addition, because the infusion of 10(-7) M GRP suppressed the somatostatin secretion, we suggest that either GRP should be excluded from the list of candidates for the noncholinergic stimulatory neurotransmitter for somatostatin secretion or that there are different mechanisms of action for endogenous and exogenous GRP.

NO mediates gastric relaxation after brief vagal stimulation in anesthetized dogs

1995 ◽  
Vol 269 (2) ◽  
pp. G255-G261 ◽  
Author(s):  
A. L. Meulemans ◽  
J. G. Eelen ◽  
J. A. Schuurkes
Keyword(s):  
Electrical Stimulation ◽  
Vagal Stimulation ◽  
Gastric Volume ◽  
Maximal Effect ◽  
Platinum Electrodes ◽  
Frequency Dependent ◽  
Vagal Nerves ◽  
Guinea Pig Stomach ◽  
Stimulation Of

In vitro studies showed that relaxations induced after vagal stimulation of the guinea pig stomach are mediated via nitric oxide (NO). The role of NO in canine gastric relaxation in response to vagal stimulation has as yet not been studied. The present study examined the influence of NG-nitro-L-arginine (L-NNA) on gastric relaxations after vagal nerve stimulation in the anesthetized dog. In beagle dogs (n = 7), the ventral and dorsal abdominal vagal nerves were connected to a pair of platinum electrodes. Gastric tone was measured by means of a barostat. Changes in gastric motility were measured with force transducers sutured on the fundus and the antrum. The cervical vagi were sectioned, and dogs were given atropine (0.2 mg/kg i.v.) and guanethidine (5 mg/kg i.v.). Electrical stimulation of the vagal trunks (19 V, 1-ms duration, for 15 s every 2 min, 1-30 Hz) induced frequency-dependent increases in volume. On the fundus, frequency-dependent relaxations could be observed (maximal effect at 5 mmHg and at 10 Hz). During electrical stimulation, the spontaneous antral contractions were completely blocked. After cessation of the stimulus, "rebound" contractions could be observed. L-NNA (5 mg/kg i.v.) completely blocked the increases in gastric volume and the relaxations on the fundus. On the antrum, however, contractions were observed during the electrical stimulation. L-Arginine (250 mg/kg i.v.) gradually restored the relaxations on electrical stimulation. This study demonstrates that NO mediates short-lasting vagally induced gastric relaxations in the anesthetized dog.

scholarly journals Electrical stimulation of the mucosa evokes slow EPSPs mediated by NK1 tachykinin receptors and by P2Y1 purinoceptors in different myenteric neurons

2009 ◽  
Vol 297 (1) ◽  
pp. G179-G186 ◽  
Author(s):  
Rachel M. Gwynne ◽  
Joel C. Bornstein
Keyword(s):  
Electrical Stimulation ◽  
Pyridoxal Phosphate ◽  
Enteric Neurons ◽  
Disulfonic Acid ◽  
Myenteric Neurons ◽  
Mrs 2179 ◽  
Neurokinin 1 ◽  
Oxide Synthase ◽  
Stimulation Of

Slow excitatory postsynaptic potentials (EPSPs) in enteric neurons arise from diverse sources, but which neurotransmitters mediate specific types of slow EPSPs is unclear. We investigated transmitters and receptors mediating slow EPSPs in myenteric neurons evoked by electrical stimulation of the mucosa in guinea pig small intestine. Segments of ileum or jejunum were dissected to allow access to the myenteric plexus adjacent to intact mucosa, in vitro. AH and S neurons were impaled with conventional intracellular electrodes. Trains of stimuli delivered to the mucosa evoked slow EPSPs in AH neurons that were blocked or depressed by the neurokinin-1 (NK1) tachykinin antagonist SR140333 (100 nM) in 10 of 11 neurons; the NK3 tachykinin receptor antagonist SR142801 (100 nM) had no effect on slow EPSPs in seven of nine AH neurons. Single pulses to the mucosa evoked fast EPSPs and slow depolarizations in S neurons. The depolarizations were divided into intermediate (durations 300–900 ms) or slow (durations 1.3–9 s) EPSPs. The slow EPSPs were blocked by pyridoxal phosphate-6-axophenyl-2–4-disulfonic acid (30 μM, N = 3) or the specific P2Y1 antagonist MRS 2179 (10 μM, N = 6) and were predominantly in anally projecting S neurons that were immunoreactive for nitric oxide synthase (NOS). In contrast, intermediate EPSPs were predominantly evoked in NOS-negative neurons; these were abolished by MRS 2179 ( N = 8). Thus activation of pathways running from the mucosa excites three different types of slow EPSP in myenteric neurons, which are mediated by either a tachykinin (NK1, AH neurons) or a purine nucleotide (P2Y1, S neurons).

Properties of synaptic inputs from myenteric neurons innervating submucosal S neurons in guinea pig ileum

2000 ◽  
Vol 278 (2) ◽  
pp. G273-G280 ◽  
Author(s):  
B. A. Moore ◽  
S. Vanner
Keyword(s):  
Guinea Pig ◽  
Myenteric Plexus ◽  
Intracellular Recordings ◽  
Guinea Pig Ileum ◽  
Myenteric Neurons ◽  
Synaptic Inputs ◽  
Stimulus Train ◽  
Stimulation Of ◽  
Double Chamber

This study examined synaptic inputs from myenteric neurons innervating submucosal neurons. Intracellular recordings were obtained from submucosal S neurons in guinea pig ileal preparations in vitro, and synaptic inputs were recorded in response to electrical stimulation of exposed myenteric plexus. Most S neurons received synaptic inputs [>80% fast (f) excitatory postsynaptic potentials (EPSP), >30% slow (s) EPSPs] from the myenteric plexus. Synaptic potentials were recorded significant distances aboral (fEPSPs, 25 mm; sEPSPs, 10 mm) but not oral to the stimulating site. When preparations were studied in a double-chamber bath that chemically isolated the stimulating “myenteric chamber” from the recording side “submucosal chamber,” all fEPSPs were blocked by hexamethonium in the submucosal chamber, but not by a combination of nicotinic, purinergic, and 5-hydroxytryptamine-3 receptor antagonists in the myenteric chamber. In 15% of cells, a stimulus train elicited prolonged bursts of fEPSPs (>30 s duration) that were blocked by hexamethonium. These findings suggest that most submucosal S neurons receive synaptic inputs from predominantly anally projecting myenteric neurons. These inputs are poised to coordinate intestinal motility and secretion.

scholarly journals Effect of Electrical Stimulation of the Vagus Nerves on Bile Secretion in Anaesthetized Sheep

1976 ◽  
Vol 29 (4) ◽  
pp. 351 ◽  
Author(s):  
MichaeI Pass ◽  
Trevor Heath
Keyword(s):  
Electrical Stimulation ◽  
Bile Salt ◽  
Maximum Rate ◽  
Vagal Stimulation ◽  
Bile Secretion ◽  
Vagus Nerves ◽  
Bile Formation ◽  
Vagal Innervation ◽  
Bicarbonate Output ◽  
Stimulation Of

Bile was collected before and during electrical stimulation of the vagus nerves in acute experiments on sheep with ligated cystic ducts. Most stimuli caused no change in: bile formation, but a 10-V, 10-Hz stimulus caused a slight increase in bicarbonate output. Neither the response to infused secretin nor the maximum rate of bile salt transpoit by liver cells changed during vagal stimulation; It was concluded that the vagal innervation of the liver is not likely to playa major role in the regulation of bile formation in sheep.

Influence of sacral nerves on the internal anal sphincter of the opossum

1987 ◽  
Vol 253 (3) ◽  
pp. G345-G350
Author(s):  
S. Rattan ◽  
R. Shah
Keyword(s):  
Anal Sphincter ◽  
Internal Anal Sphincter ◽  
Nicotinic Receptors ◽  
Inhibitory Neurons ◽  
Inhibitory Pathway ◽  
Release Of Acetylcholine ◽  
Adrenergic Antagonists ◽  
Sacral Nerves ◽  
Alpha Chloralose ◽  
Stimulation Of

The purpose of the present studies is to 1) compare the effects of stimulation of different sacral nerves (S1-S5) on internal anal sphincter (IAS) pressures and 2) examine the nature of synaptic transmission in the sacral inhibitory pathway to the IAS. Pressures from the IAS of alpha-chloralose-anesthetized opossums were recorded using a low-compliance continuously perfused catheter assembly. Electrical stimulation of the third and fourth sacral nerves (S3 and S4) caused frequency-dependent IAS relaxation, whereas stimulation of other sacral nerves was without significant effect on the IAS. Relaxation of the IAS in response to S4 stimulation was not significantly modified by atropine, pirenzepine dihydrochloride, hexamethonium chloride, or adrenergic antagonists. However, a combination of either atropine and hexamethonium or pirenzepine and hexamethonium caused a significant antagonism of sacral nerve-stimulated relaxation without modifying the inhibitory responses of local transmural nerve stimulation and isoproterenol. From these studies we conclude that 1) in the opossum the sacral nerves primarily exert inhibitory influences on the IAS and 2) the sacral inhibitory pathway involves the release of acetylcholine from preganglionic fibers, which in turn causes the activation of both muscarinic (M1) and nicotinic receptors on postganglionic, noncholinergic, nonadrenergic inhibitory neurons.

Effect of thoracic vagotomy and vagal stimulation on esophageal function.

1978 ◽  
Vol 234 (4) ◽  
pp. E359 ◽  
Author(s):  
J J Kravitz ◽  
W J Snape ◽  
S Cohen
Keyword(s):  
Electrical Stimulation ◽  
Vagal Stimulation ◽  
Esophageal Function ◽  
Primary Peristalsis ◽  
Vagal Innervation ◽  
Relaxation Responses ◽  
Secondary Peristalsis ◽  
Thoracic Vagotomy ◽  
Upper Thoracic ◽  
Stimulation Of

The purpose of this study was to determine the effect of thoracic vagotomy and thoracic vagal stimulation upon esophageal peristalsis and lower esophageal sphincter (LES) function in the opossum. The thoracic portion of the vagus nerve was sectioned in the upper or lower thorax. Bilateral, but not unilateral, thoracic vagotomy above the level of the heart abolished peristalsis and LES relaxation in response to swallowing or cervical vagal electrical stimulation. Thoracic vagotomy at the level of the ventricle or below did not alter either peristalsis or LES relaxation during swallowing or cervical vagal stimulation. Secondary peristalsis and its associated LES relaxation was unaltered by thoracic vagotomy at any level. Electrical stimulation of the distal end of the upper thoracic vagus elicited both peristalsis and LES relaxation. Electrical stimulation of the distal end of the lower thoracic vagus elicited both peristalsis and LES relaxation. Electrical stimulation of the distal end of the lower thoracic vagus, as well as stimulation of the vagal branches to the terminal esophagus, gave only LES relaxation. These studies suggest that: a) the major extrinsic vagal innervation mediating primary peristalsis terminates in the upper portion of the esophagus, whereas the vagal innervation mediating LES relaxation responses are present throughout the length of the esophagus; and b) secondary peristalsis and its associated LES relaxation occurs independent of extrinsic vagal innervation.

Discrete responses of myenteric neurons to structural and functional damage by neurotoxins in vitro

2009 ◽  
Vol 297 (1) ◽  
pp. G228-G239 ◽  
Author(s):  
Sandra Lourenssen ◽  
Kurtis G. Miller ◽  
Michael G. Blennerhassett
Keyword(s):  
Hydrogen Peroxide ◽  
Neurotransmitter Release ◽  
Caspase 3 ◽  
Neuronal Survival ◽  
Neuronal Loss ◽  
Annexin V ◽  
Ach Release ◽  
Myenteric Neurons ◽  
Release Of Acetylcholine

Damage to the enteric nervous system is implicated in human disease and animal models of inflammatory bowel disease, diabetes, and Parkinson's disease, but the mechanism of death and the response of surviving neurons are poorly understood. We explored this in a coculture model of myenteric neurons, glia, and smooth muscle during exposure to the established or potential neurotoxins botulinum A, hydrogen peroxide, and acrylamide. Neuronal survival, axonal degeneration and regeneration, and neurotransmitter release were assessed during acute exposure (0–24 h) to neurotoxin and subsequent recovery (96–144 h). Unique and selective responses to each neurotoxin were found with acrylamide (0.5–2.0 mM) causing a 30% decrease in axon number without neuronal loss, whereas hydrogen peroxide (1–200 μM) caused a parallel loss in both axon and neuron number. Immunoblotting identified the loss of synaptic vesicle proteins that paralleled axon damage and was associated with marked suppression of depolarization-induced release of acetylcholine (ACh). The caspase inhibitor zVAD, but not DEVD, significantly prevented neuronal death, implying a largely caspase-3/7-independent mechanism of apoptotic death that was supported by staining for annexin V and cleaved caspase-3. In contrast, botulinum A (2 μg/ml) caused a 40% decrease in ACh release without effect on neuronal survival or axon structure. By 96 h after exposure to acrylamide or hydrogen peroxide, axon number was restored to or even surpassed the level of time-matched controls, regardless of partial neuronal loss, but ACh release remained markedly suppressed. Neural responses to toxic factors are initially unique but then converge upon robust axonal regeneration, whereas neurotransmitter release is both vulnerable to damage and slow to recover.

scholarly journals Oxytocin regulates gastrointestinal motility, inflammation, macromolecular permeability, and mucosal maintenance in mice

2014 ◽  
Vol 307 (8) ◽  
pp. G848-G862 ◽  
Author(s):  
Martha G. Welch ◽  
Kara G. Margolis ◽  
Zhishan Li ◽  
Michael D. Gershon
Keyword(s):  
Neuronal Development ◽  
Intestinal Inflammation ◽  
Experimental Colitis ◽  
Enteric Neurons ◽  
Developmentally Regulated ◽  
Mucosal Permeability ◽  
Myenteric Neurons ◽  
Neuronal Regulation ◽  
Macromolecular Permeability

Enteric neurons express oxytocin (OT); moreover, enteric neurons and enterocytes express developmentally regulated OT receptors (OTRs). Although OT (with secretin) opposes intestinal inflammation, physiological roles played by enteric OT/OTR signaling have not previously been determined. We tested hypotheses that OT/OTR signaling contributes to enteric nervous system (ENS)-related gastrointestinal (GI) physiology. GI functions and OT effects were compared in OTR-knockout (OTRKO) and wild-type (WT) mice. Stool mass and water content were greater in OTRKO mice than in WT. GI transit time in OTRKO animals was faster than in WT; OT inhibited in vitro generation of ENS-dependent colonic migrating motor complexes in WT but not in OTRKO mice. Myenteric neurons were hyperplastic in OTRKO animals, and mucosal exposure to cholera toxin (CTX) in vitro activated Fos in more myenteric neurons in OTRKO than WT than in WT mice; OT inhibited the CTX response in WT but not in OTRKO mice. Villi and crypts were shorter in OTRKO than in WT mice, and transit-amplifying cell proliferation in OTRKO crypts was deficient. Macromolecular intestinal permeability in OTRKO was greater than WT mice, and experimental colitis was more severe in OTRKO mice; moreover, OT protected WT animals from colitis. Observations suggest that OT/OTR signaling acts as a brake on intestinal motility, decreases mucosal activation of enteric neurons, and promotes enteric neuronal development and/or survival. It also regulates proliferation of crypt cells and mucosal permeability; moreover OT/OTR signaling is protective against inflammation. Oxytocinergic signaling thus appears to play an important role in multiple GI functions that are subject to neuronal regulation.

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