scholarly journals Neural pathways regulating Brunner's gland secretion in guinea pig duodenum in vitro

2000 ◽  
Vol 279 (5) ◽  
pp. G910-G917 ◽  
Author(s):  
Beverley A. Moore ◽  
David Kim ◽  
Stephen Vanner
Keyword(s):  
Electrical Stimulation ◽  
Guinea Pig ◽  
Nerve Fibers ◽  
Neural Pathways ◽  
Brunner's Glands ◽  
Brunner’S Glands ◽  
Perivascular Nerves ◽  
Acinar Lumen ◽  
Stimulation Of

This study examined the neural pathways innervating Brunner's glands using a novel in vitro model of acinar secretion from Brunner's glands in submucosal preparations from the guinea pig duodenum. Neural pathways were activated by focal electrical stimulation and excitatory agonists, and videomicroscopy was used to monitor dilation of acinar lumen. Electrical stimulation of perivascular nerves evoked large dilations that were blocked by TTX (1 μM) or the muscarinic receptor antagonist 4-diphenylacetoxy- N-(2-chloroethyl)-piperidine hydrochloride (1 μM). The nicotinic agonist 1,1-dimethyl-4-phenylpiperazinium iodide (100 μM) had no effect, and the nerve-evoked responses were not inhibited by hexamethonium (200 μM). Dilations were abolished in preparations from chronically vagotomized animals. Activation of submucosal ganglia significantly dilated submucosal arterioles but not Brunner's glands. Effects of electrical stimulation of perivascular and submucosal nerves were not altered by guanethidine. Capsaicin and substance P also dilated arterioles but had no effect on Brunner's glands. Cholinergic (choline acetyltransferase-immunoreactive) nerve fibers were found in Brunner's glands. These findings demonstrate that Brunner's glands are innervated by cholinergic vagal fibers but not by capsaicin-sensitive or intrinsic enteric nerves.

Potassium currents regulating secretion from Brunner's glands in guinea pig duodenum

2004 ◽  
Vol 286 (3) ◽  
pp. G377-G384 ◽  
Author(s):  
Jason Kovac ◽  
Beverley Moore ◽  
Stephen Vanner
Keyword(s):  
Guinea Pig ◽  
Basolateral Membrane ◽  
Acinar Cells ◽  
Resting Membrane Potential ◽  
Channel Blockers ◽  
Membrane Hyperpolarization ◽  
Brunner's Glands ◽  
Brunner’S Glands ◽  
External K

This study examined the role of outward K+ currents in the acinar cells underlying secretion from Brunner's glands in guinea pig duodenum. Intracellular recordings were made from single acinar cells in intact acini in in vitro submucosal preparations, and videomicroscopy was employed in the same preparation to correlate these measures with secretion. Mean resting membrane potential was -74 mV and was depolarized by high external K+ (20 mM) and the K+ channel blockers 4-aminopyridine (4-AP), quinine, and clotrimazole. The cholinergic agonist carbachol (60–2,000 nM; EC50 = 200 nM) caused a concentration-dependent initial hyperpolarization of the membrane and an associated decrease in input resistance. This hyperpolarization was significantly decreased by 20 mM external K+ or membrane hyperpolarization and increased by 1 mM external K+ or membrane depolarization. It was blocked by the K+ channel blockers tetraethylammonium (TEA), 4-AP, quinine, and clotrimazole but not iberiotoxin. When videomicroscopy was employed to measure dilation of acinar lumen in the same preparation, carbachol-evoked dilations were altered in a parallel fashion when external K+ was altered. The dilations were also blocked by the K+ channel blockers TEA, 4-AP, quinine, and clotrimazole but not iberiotoxin. These findings suggest that activation of outward K+ currents is fundamental to the initiation of secretion from these glands, consistent with the model of K+ efflux from the basolateral membrane providing the driving force for secretion. The pharmacological profile suggests that these K+ channels belong to the intermediate conductance group.

A novel in vitro model of Brunner's gland secretion in the guinea pig duodenum

2000 ◽  
Vol 278 (3) ◽  
pp. G477-G485 ◽  
Author(s):  
Beverley A. Moore ◽  
Gerald P. Morris ◽  
Stephen Vanner
Keyword(s):  
Guinea Pig ◽  
In Vitro Model ◽  
Gland Secretion ◽  
Luminal Diameter ◽  
Brunner's Glands ◽  
Brunner’S Glands ◽  
Brunner’S Gland ◽  
Vitro Model ◽  
Brunner's Gland

A novel in vitro model that combined functional and morphological techniques was employed to directly examine pathways regulating Brunner's gland secretion in isolation from epithelium. In vitro submucosal preparations were dissected from guinea pig duodenum. A videomicroscopy technique was used to measure changes in luminal diameter of glandular acini as an index of activation of secretion. Carbachol elicited concentration-dependent dilations of the lumen (EC50= 2 μM) by activating muscarinic receptors on acinar cells. Ultrastructural and histological analyses demonstrated that dilation was accompanied by single and compound exocytosis of mucin-containing granules and the accumulation of mucoid material within the lumen. Inflammatory mediators (histamine, PGE1, PGE2) and intestinal hormones (CCK, gastrin, vasoactive intestinal polypeptide, secretin) also stimulated glandular secretion, whereas activation of submucosal secretomotor neurons by 5-hydroxytryptamine did not. This study directly demonstrates that multiple hormonal, inflammatory, and neurocrine agents activate Brunner's glands, whereas many have dissimilar effects on the epithelium. This suggests that Brunner's glands are regulated by pathways that act both in parallel to and in isolation from those controlling epithelial secretion.

Pharmacological modulation of cholinergic neurotransmission in guinea pig trachea in vitro

1980 ◽  
Vol 58 (7) ◽  
pp. 810-822 ◽  
Author(s):  
Thomas R. Jones ◽  
John T. Hamilton ◽  
Neville M. Lefcoe
Keyword(s):  
Electrical Stimulation ◽  
Guinea Pig ◽  
Low Frequency ◽  
Electrical Field Stimulation ◽  
Prostaglandin E ◽  
Cholinergic Nerves ◽  
Experimental Conditions ◽  
Cholinergic Neurotransmission ◽  
Stimulation Of

Electrical (field) stimulation of the isolated guinea pig trachea with normal intrinsic tone produced a biphasic response which consisted of an initial (cholinergic) contraction followed by (adrenergic and nonadrenergic) relaxation. Treatment of the tissue with the prostaglandin synthetase inhibitor indomethacin (2.8–5.6 μM) removed intrinsic tone and increased the responsiveness of the tissue to stimulation of cholinergic nerves and to exogenous acetylcholine. Indomethacin-relaxed tracheae were subsequently used to study cholinergic neurotransmission because under these experimental conditions only the contractile component of the response to electrical stimulation was observed. The β adrenoceptor blocking agents dl-propranolol and sotalol and the adrenergic neuron blocking agent guanethidine produced further enhancement of the contraction to electrical stimulation at low frequency (1–10 Hz). Prostaglandin E1, l-noradrenaline, l-adrenaline, salbutamol, phenylephrine, and phentolamine selectively attenuated the contractions to electrical stimulation in concentrations which did not significantly alter the matched responses to exogenous acetylcholine. The selective depressant effect of l-noradrenaline, l-adrenaline, salbutamol, phenylephrine, and phentolamine but not prostaglandin E1 were blocked by dl-propranolol or sotalol. The present results demonstrate that responses to stimulation of cholinergic nerves were altered by (1) prostaglandins and inhibitors of their synthesis, (2) neurally released adrenergic transmitter, and (3) exogenously added β adrenoceptor agonists. The possibility that prostaglandins and adrenergic neurotransmitter may modulate cholinergic neurotransmission at both pre- and post-junctional sites is hypothesized. It is proposed that more attention should be paid to the role of cholinergic transmission and its modulation in the studies of airway smooth muscle.

scholarly journals Establishment of a New Device for Electrical Stimulation of Non-Degenerative Cartilage Cells In Vitro

2021 ◽  
Vol 22 (1) ◽  
pp. 394
Author(s):  
Simone Krueger ◽  
Alexander Riess ◽  
Anika Jonitz-Heincke ◽  
Alina Weizel ◽  
Anika Seyfarth ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Electric Fields ◽  
Cartilage Tissue ◽  
Type I ◽  
Dependent Manner ◽  
New Device ◽  
Alternating Electric Fields ◽  
Cartilage Cells ◽  
Stimulation Of

In cell-based therapies for cartilage lesions, the main problem is still the formation of fibrous cartilage, caused by underlying de-differentiation processes ex vivo. Biophysical stimulation is a promising approach to optimize cell-based procedures and to adapt them more closely to physiological conditions. The occurrence of mechano-electrical transduction phenomena within cartilage tissue is physiological and based on streaming and diffusion potentials. The application of exogenous electric fields can be used to mimic endogenous fields and, thus, support the differentiation of chondrocytes in vitro. For this purpose, we have developed a new device for electrical stimulation of chondrocytes, which operates on the basis of capacitive coupling of alternating electric fields. The reusable and sterilizable stimulation device allows the simultaneous use of 12 cavities with independently applicable fields using only one main supply. The first parameter settings for the stimulation of human non-degenerative chondrocytes, seeded on collagen type I elastin-based scaffolds, were derived from numerical electric field simulations. Our first results suggest that applied alternating electric fields induce chondrogenic re-differentiation at the gene and especially at the protein level of human de-differentiated chondrocytes in a frequency-dependent manner. In future studies, further parameter optimizations will be performed to improve the differentiation capacity of human cartilage cells.

Effects of Electrical Stimulation of the Superior Cervical Ganglion on Cochlear Blood Flow in Guinea Pig

1993 ◽  
Vol 113 (2) ◽  
pp. 146-151 ◽  
Author(s):  
Tian-Ying Ren ◽  
E. Laurikainen ◽  
W. S. Quirk ◽  
J. M. Miller ◽  
A. L. Nuttall
Keyword(s):  
Blood Flow ◽  
Electrical Stimulation ◽  
Guinea Pig ◽  
Superior Cervical Ganglion ◽  
Cochlear Blood Flow ◽  
Cervical Ganglion ◽  
Stimulation Of

Protective role of epithelium in the guinea pig airway

1989 ◽  
Vol 66 (4) ◽  
pp. 1547-1552 ◽  
Author(s):  
M. Munakata ◽  
I. Huang ◽  
W. Mitzner ◽  
H. Menkes
Keyword(s):  
Guinea Pig ◽  
Protective Role ◽  
Airway Epithelial ◽  
Serosal Side ◽  
Epithelial Surface ◽  
Airway Responses ◽  
Airway Tone ◽  
Stimulation Of

We developed an in vitro system to assess the role of the epithelium in regulating airway tone using the intact guinea pig trachea (J. Appl. Physiol. 64: 466–471, 1988). This method allows us to study the response of the airway when its inner epithelial surface or its outer serosal surface is stimulated independently. Using this system we evaluated how the presence of intact epithelium can affect pharmacological responsiveness. We first examined responses of tracheae with intact epithelium to histamine, acetylcholine, and hypertonic KCl when stimulated from the epithelial or serosal side. We then examined the effect of epithelial denudation on the responses to these agonists. With an intact epithelium, stimulation of the inner epithelial side always caused significantly smaller changes in diameter than stimulation of the outer serosal side. After mechanical denudation of the epithelium, these differences were almost completely abolished. In the absence of intact epithelium, the trachea was 35-fold more sensitive to histamine and 115-fold more sensitive to acetylcholine when these agents were applied to the inner epithelial side. In addition, the presence of an intact epithelium almost completely inhibited any response to epithelial side challenge with hypertonic KCl. These results indicate that the airway epithelial layer has a potent protective role in airway responses to luminal side stimuli, leading us to speculate that changes in airway reactivity measured in various conditions including asthma may result in part from changes in epithelial function.

ATP concentrations and muscle tension increase linearly with muscle contraction

2003 ◽  
Vol 95 (2) ◽  
pp. 577-583 ◽  
Author(s):  
Jianhua Li ◽  
Nicholas C. King ◽  
Lawrence I. Sinoway
Keyword(s):  
Skeletal Muscle ◽  
Electrical Stimulation ◽  
Muscle Contraction ◽  
Motor Nerve ◽  
Muscle Tension ◽  
Nerve Fibers ◽  
Ventral Root ◽  
Ventral Roots ◽  
Root Stimulation ◽  
Stimulation Of

Previous studies have suggested that activation of ATP-sensitive P2X receptors in skeletal muscle play a role in mediating the exercise pressor reflex (Li J and Sinoway LI. Am J Physiol Heart Circ Physiol 283: H2636–H2643, 2002). To determine the role ATP plays in this reflex, it is necessary to examine whether muscle interstitial ATP (ATPi) concentrations rise with muscle contraction. Accordingly, in this study, muscle contraction was evoked by electrical stimulation of the L7 and S1 ventral roots of the spinal cord in 12 decerebrate cats. Muscle ATPi was collected from microdialysis probes inserted in the muscle. ATP concentrations were determined by the HPLC method. Electrical stimulation of the ventral roots at 3 and 5 Hz increased mean arterial pressure by 13 ± 2 and 16 ± 3 mmHg ( P < 0.05), respectively, and it increased ATP concentration in contracting muscle by 150% ( P < 0.05) and 200% ( P < 0.05), respectively. ATP measured in the opposite control limb did not rise with ventral root stimulation. Section of the L7 and S1 dorsal roots did not affect the ATPi seen with 5-Hz ventral root stimulation. Finally, ventral roots stimulation sufficient to drive motor nerve fibers did not increase ATP in previously paralyzed cats. Thus ATPi is not largely released from sympathetic or motor nerves and does not require an intact afferent reflex pathway. We conclude that ATPi is due to the release of ATP from contracting skeletal muscle cells.

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