Neural regulation of slow-wave frequency in the murine gastric antrum

2006 ◽  
Vol 290 (3) ◽  
pp. G486-G495 ◽  
Author(s):  
Abigail S. Forrest ◽  
Tamás Ördög ◽  
Kenton M. Sanders
Keyword(s):  
Motor Neurons ◽  
Slow Wave ◽  
Electrical Field Stimulation ◽  
Slow Waves ◽  
Wave Frequency ◽  
Field Stimulation ◽  
Neural Regulation ◽  
Electrical Field ◽  
Chronotropic Response ◽  
Chronotropic Effects

Gastric peristaltic contractions are driven by electrical slow waves modulated by neural and humoral inputs. Excitatory neural input comes primarily from cholinergic motor neurons, but ACh causes depolarization and chronotropic effects that might disrupt the normal proximal-to-distal spread of gastric slow waves. We used intracellular electrical recording techniques to study cholinergic responses in stomach tissues from wild-type and W/W V mice. Electrical field stimulation (5 Hz) enhanced slow-wave frequency. These effects were abolished by atropine and the muscarinic M3-receptor antagonist 4-diphenylacetoxy- N-methylpiperidine methiodide. ACh released from nerves did not depolarize antral muscles. At higher rates of stimulation (10 Hz), chronotropic effects were mediated by ACh and a noncholinergic transmitter and blocked by muscarinic antagonists and neurokinin (NK1 and NK2)-receptor antagonists. Neostigmine enhanced slow-wave frequency, suggesting that the frequency of antral pacemakers is kept low by efficient metabolism of ACh. Neostigmine had no effect on slow-wave frequency in muscles of W/W v mice, which lack intramuscular interstitial cells of Cajal (ICC-IM). These muscles also showed no significant chronotropic response to 5-Hz electrical field stimulation or the cholinergic agonist carbachol. The data suggest that the chronotropic effects of cholinergic nerve stimulation occur via ICC-IM in the murine stomach. The capacity of gastric muscles to metabolize ACh released from enteric motor neurons contributes to the maintenance of the proximal-to-distal slow-wave frequency gradient in the murine stomach. ICC-IM play a critical role in neural regulation of gastric motility, and ICC-IM become the dominant pacemaker cells during sustained cholinergic drive.

scholarly journals Prostaglandin regulation of gastric slow waves and peristalsis

2009 ◽  
Vol 296 (6) ◽  
pp. G1180-G1190 ◽  
Author(s):  
Abigail S. Forrest ◽  
Grant W. Hennig ◽  
Sari Jokela-Willis ◽  
Chong Doo Park ◽  
Kenton M. Sanders
Keyword(s):  
Slow Wave ◽  
Slow Waves ◽  
Wave Frequency ◽  
Functional Coupling ◽  
Receptor Agonists ◽  
Gastric Corpus ◽  
Gastric Peristalsis ◽  
Chronotropic Effects ◽  
Cells Of Cajal ◽  
The Impact

Gastric emptying depends on functional coupling of slow waves between the corpus and antrum, to allow slow waves initiated in the gastric corpus to propagate to the pyloric sphincter and generate gastric peristalsis. Functional coupling depends on a frequency gradient where slow waves are generated at higher frequency in the corpus and drive the activity of distal pacemakers. Simultaneous intracellular recording from corpus and antrum was used to characterize the effects of PGE2 on slow waves in the murine stomach. PGE2 increased slow-wave frequency, and this effect was mimicked by EP3, but not by EP2, receptor agonists. Chronotropic effects were due to EP3 receptors expressed by intramuscular interstitial cells of Cajal because these effects were not observed in W/W V mice. Although the integrated chronotropic effects of EP3 receptor agonists were deduced from electrophysiological experiments, no clear evidence of functional uncoupling was observed with two-point electrical recording. Gastric peristalsis was also monitored by video imaging and spatiotemporal maps to study the impact of chronotropic agonists on propagating contractions. EP3 receptor agonists increased the frequency of peristaltic contractions and caused ectopic sites of origin and collisions of peristaltic waves. The impact of selective regional application of chronotropic agonists was investigated by use of a partitioned bath. Antral slow waves followed enhanced frequencies induced by stimulation of the corpus, and corpus slow waves followed when slow-wave frequency was elevated in the antrum. This demonstrated reversal of slow-wave propagation with selective antral chronotropic stimulation. These studies demonstrate the impact of chronotropic agonists on regional intrinsic pacemaker frequency and integrated gastric peristalsis.

Different responsiveness of excitatory and inhibitory enteric motor neurons in the human esophagus to electrical field stimulation and to nicotine

2004 ◽  
Vol 287 (1) ◽  
pp. G299-G306 ◽  
Author(s):  
Asensio A. González ◽  
Ricard Farré ◽  
Pere Clavé
Keyword(s):  
Motor Neurons ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Electrical Field Stimulation ◽  
Field Stimulation ◽  
Weak Contraction ◽  
Electrical Field ◽  
Esophageal Sphincter ◽  
Human Esophagus ◽  
Cholinergic Contraction

To compare electrical field stimulation (EFS) with nicotine in the stimulation of excitatory and inhibitory enteric motoneurons (EMN) in the human esophagus, circular lower esophageal sphincter (LES), and circular and longitudinal esophageal body (EB) strips from 20 humans were studied in organ baths. Responses to EFS or nicotine (100 μM) were compared in basal conditions, after NG-nitro-l-arginine (l-NNA; 100 μM), and after l-NNA and apamin (1 μM). LES strips developed myogenic tone enhanced by TTX (5 μM) or l-NNA. EFS-LES relaxation was abolished by TTX, unaffected by hexamethonium (100 μM), and enhanced by atropine (3 μM). Nicotine-LES relaxation was higher than EFS relaxation, reduced by TTX or atropine, and blocked by hexamethonium. After l-NNA, EFS elicited a strong cholinergic contraction in circular LES and EB, and nicotine elicited a small relaxation in LES and no contractile effect in EB. After l-NNA and apamin, EFS elicited a strong cholinergic contraction in LES and EB, and nicotine elicited a weak contraction amounting to 6.64 ± 3.19 and 9.20 ± 5.51% of that induced by EFS. EFS elicited a contraction in longitudinal strips; after l-NNA and apamin, nicotine did not induce any response. Inhibitory EMN tonically inhibit myogenic LES tone and are efficiently stimulated both by EFS and nicotinic acetylcholine receptors (nAChRs) located in somatodendritic regions and nerve terminals, releasing nitric oxide and an apamin-sensitive neurotransmitter. In contrast, although esophageal excitatory EMN are efficiently stimulated by EFS, their stimulation through nAChRs is difficult and causes weak responses, suggesting the participation of nonnicotinic mechanisms in neurotransmission to excitatory EMN in human esophagus.

Further studies on the motor response of the human isolated urinary bladder to tachykinins, capsaicin and electrical field stimulation

1989 ◽  
Vol 20 (5) ◽  
pp. 663-669 ◽  
Author(s):  
Carlo Alberto Maggi ◽  
Riccardo Patacchini ◽  
Paolo Santicioli ◽  
Damiano Turini ◽  
Gabriele Barbanti ◽  
...  
Keyword(s):  
Urinary Bladder ◽  
Motor Response ◽  
Electrical Field Stimulation ◽  
Field Stimulation ◽  
Electrical Field

Pharmacologic responses of the mouse urinary bladder

Open Medicine ◽  
2009 ◽  
Vol 4 (2) ◽  
pp. 192-197 ◽  
Author(s):  
A. Canda ◽  
Christopher Chapple ◽  
Russ Chess-Williams
Keyword(s):  
Nitric Oxide ◽  
Urinary Bladder ◽  
Electrical Field Stimulation ◽  
Inhibitory Effect ◽  
Minor Role ◽  
Detrusor Muscle ◽  
Field Stimulation ◽  
Muscarinic Agonists ◽  
Electrical Field ◽  
M3 Receptor

AbstractThe aim of the study was to determine pathways involved in contraction and relaxation of the mouse urinary bladder. Mouse bladder strips were set up in gassed Krebs-bicarbonate solution and responses to various drugs and electrical field stimulation were obtained. Isoprenaline (b-receptor agonist) caused a 63% inhibition of carbachol precontracted detrusor (EC50=2nM). Carbachol caused contraction (EC50=0.3µM), responses were antagonised more potently by 4-DAMP (M3-antagonist) than methoctramine (M2-antagonist). Electrical field stimulation caused contraction, which was inhibited by atropine (60%) and less by guanethidine and α,β-methylene-ATP. The neurogenic responses were not potentiated by inhibition of nitric oxide synthase. Presence of an intact urothelium significantly depressed responses to carbachol (p=0.02) and addition of indomethacin and L-NNA to remove prostaglandin and nitric oxide production respectively did not prevent the inhibitory effect of the urothelium. In conclusion, b-receptor agonists cause relaxation and muscarinic agonists cause contraction via the M3-receptor. Acetylcholine is the main neurotransmitter causing contraction while nitric oxide has a minor role. The mouse and human urothelium are similar in releasing a factor that inhibits contraction of the detrusor muscle which is unidentified but is not nitric oxide or a prostaglandin. Therefore, the mouse may be used as a model to study the lower urinary tract.

Treatment of gastric ulcers and diarrhea with the Amazonian herbal medicine sangre de grado

2000 ◽  
Vol 279 (1) ◽  
pp. G192-G200 ◽  
Author(s):  
Mark J. S. Miller ◽  
Wallace K. MacNaughton ◽  
Xiao-Jing Zhang ◽  
Jane H. Thompson ◽  
Randi M. Charbonnet ◽  
...  
Keyword(s):  
Herbal Medicine ◽  
Cost Effective ◽  
Electrical Field Stimulation ◽  
Skin Lesions ◽  
Gastric Ulcers ◽  
Myeloperoxidase Activity ◽  
Field Stimulation ◽  
Electrical Field ◽  
Ussing Chambers ◽  
Cost Effective Treatment

Sangre de grado is an Amazonian herbal medicine used to facilitate the healing of gastric ulcers and to treat gastritis, diarrhea, skin lesions, and insect stings. This study was designed to evaluate the gastrointestinal applications. Gastric ulcers were induced in rats by brief serosal exposure of the fundus to acetic acid (80%). Sangre de grado was administered in drinking water at 1:1,000 and 1:10,000 dilutions from the postoperative period to day 7. Guinea pig ileum secretory responses to capsaicin, electrical field stimulation, and the neurokinin-1 (NK-1) agonist [Sar9,Met(O2)11]substance P were examined in Ussing chambers. Sangre de grado facilitated the healing of experimental gastric ulcer, reducing myeloperoxidase activity, ulcer size, and bacterial content of the ulcer. The expression of proinflammatory genes tumor necrosis factor-α, inducible nitric oxide synthase (iNOS), interleukin (IL)-1β, IL-6, and cyclooxygenase-2 was upregulated by ulcer induction but reduced by sangre de grado treatment, particularly iNOS and IL-6. In Ussing chambers, sangre de grado impaired the secretory response to capsaicin but not to electrical field stimulation or the NK-1 agonist. We conclude that sangre de grado is a potent, cost-effective treatment for gastrointestinal ulcers and distress via antimicrobial, anti-inflammatory, and sensory afferent-dependent actions.

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