Different response of mucosal mast cells in rat jejunum to electrical stimulation of the cervical vagal nerves depending on sex

1997 ◽  
Vol 382 (3) ◽  
pp. 157 ◽  
Author(s):  
T. Gottwald ◽  
H.-D. Becker ◽  
R. H. Stead
Keyword(s):  
Electrical Stimulation ◽  
Mast Cells ◽  
Rat Jejunum ◽  
Mucosal Mast Cells ◽  
Vagal Nerves ◽  
Different Response ◽  
Stimulation Of

Mucosal mast cells are involved in CCK disruption of MMC in the rat intestine

1998 ◽  
Vol 275 (1) ◽  
pp. G63-G67 ◽  
Author(s):  
Carme Juanola ◽  
Magda Giralt ◽  
Marcel Jiménez ◽  
Marisabel Mourelle ◽  
Patri Vergara
Keyword(s):  
Mast Cell ◽  
Small Intestine ◽  
Mast Cells ◽  
Control Group ◽  
Rat Intestine ◽  
Pancreatic Acini ◽  
Mast Cell Stabilizer ◽  
Mucosal Mast Cells ◽  
Stimulation Of ◽  
Cck Release

Our aim was to determine if mucosal mast cells could be activated by endogenous CCK and, as a consequence, mediate CCK actions in the small intestine. Rats were prepared for electromyography to record electrical activity in the small intestine. In another group of animals, the duodenum was perfused to measure rat mast cell protease II (RMCP II) as indicative of mast cell degranulation. Endogenous CCK release was induced by administration of soybean trypsin inhibitor (SBTI) in conscious rats or by intraduodenal perfusion of ovalbumin hydrolysate (OVH) in anesthetized rats. CCK concentration was measured by bioassay on pancreatic acini. SBTI in control rats disrupted migrating motor complexes (MMC) for >40 min. In rats treated with the mast cell stabilizer ketotifen, SBTI did not induce any change in the MMC pattern. RMCP II concentration in the duodenal perfusate significantly increased after OVH. Perfusate from ketotifen-treated animals did not show any significant increase in RMCP II values during OVH perfusion, although CCK plasma concentration was not different from the control group. Furthermore, infusion of the CCK-B receptor antagonist L-365,260 significantly blocked the increase of RMCP II concentration after OVH. Our results indicate that mucosal mast cells are degranulated by endogenous CCK release through stimulation of CCK-B receptors. Therefore mucosal mast cells participate in CCK intestinal actions.

Electrical stimulation of the vagus nerve modulates the histamine content of mast cells in the rat jejunal mucosa

Neuroreport ◽  
1995 ◽  
Vol 7 (1) ◽  
pp. 313-317 ◽  
Author(s):  
Thomas P. Gottwald ◽  
Bryan R. Hewlett ◽  
Sárka Lhoták ◽  
Ron H. Stead
Keyword(s):  
Electrical Stimulation ◽  
Mast Cells ◽  
Vagus Nerve ◽  
Histamine Content ◽  
Jejunal Mucosa ◽  
Stimulation Of

Relationships between permeable vessels, nerves, and mast cells in rat cutaneous neurogenic inflammation

1990 ◽  
Vol 68 (6) ◽  
pp. 2305-2311 ◽  
Author(s):  
J. N. Baraniuk ◽  
M. L. Kowalski ◽  
M. A. Kaliner
Keyword(s):  
Electrical Stimulation ◽  
Mast Cells ◽  
Neurogenic Inflammation ◽  
Sensory Nerve ◽  
Nerve Fibers ◽  
Sensory Nerves ◽  
Neurokinin A ◽  
Rat Skin ◽  
Protein Extravasation ◽  
Stimulation Of

Electrical stimulation of rat sensory nerves produces cutaneous vasodilation and plasma protein extravasation, a phenomenon termed “neurogenic inflammation”. Rat skin on the dorsum of the paw developed neurogenic inflammation after electrical stimulation of the saphenous nerve. In tissue sections, the extravasation of the supravital dye monastral blue B identified permeable vessels. Mast cells were identified by toluidine blue stain. Permeable vessels were significantly more dense in the superficial 120 microns of the dermis than in the deeper dermis, whereas mast cells were significantly more frequent in the deeper dermis. The relationships between nociceptive sensory nerve fibers, permeable vessels, and mast cells were examined by indirect immunohistochemistry for calcitonin gene-related peptide (CGRP), neurokinin A (NKA), and substance P (SP). CGRP-, NKA-, and SP-containing nerves densely innervated the superficial dermis and appeared to innervate the vessels that became permeable during neurogenic inflammation. In contrast, mast cells were not associated with either permeable vessels or nerve fibers. These data suggest that electrical stimulation of rat sensory nerves produces vascular permeability by inducing the release of neuropeptides that may directly stimulate the superficial vascular bed. Mast cells may not be involved in this stage of cutaneous neurogenic inflammation in rat skin.

scholarly journals Innervation of enteric mast cells by primary spinal afferents in guinea pig and human small intestine

2014 ◽  
Vol 307 (7) ◽  
pp. G719-G731 ◽  
Author(s):  
Guo-Du Wang ◽  
Xi-Yu Wang ◽  
Sumei Liu ◽  
Meihua Qu ◽  
Yun Xia ◽  
...  
Keyword(s):  
Nervous System ◽  
Mast Cell ◽  
Small Intestine ◽  
Electrical Stimulation ◽  
Mast Cells ◽  
Guinea Pig ◽  
Mast Cell Protease ◽  
Human Small Intestine ◽  
Neurokinin 1 ◽  
Stimulation Of

Mast cells express the substance P (SP) neurokinin 1 receptor and the calcitonin gene-related peptide (CGRP) receptor in guinea pig and human small intestine. Enzyme-linked immunoassay showed that activation of intramural afferents by antidromic electrical stimulation or by capsaicin released SP and CGRP from human and guinea pig intestinal segments. Electrical stimulation of the afferents evoked slow excitatory postsynaptic potentials (EPSPs) in the enteric nervous system. The slow EPSPs were mediated by tachykinin neurokinin 1 and CGRP receptors. Capsaicin evoked slow EPSP-like responses that were suppressed by antagonists for protease-activated receptor 2. Afferent stimulation evoked slow EPSP-like excitation that was suppressed by mast cell-stabilizing drugs. Histamine and mast cell protease II were released by 1) exposure to SP or CGRP, 2) capsaicin, 3) compound 48/80, 4) elevation of mast cell Ca2+ by ionophore A23187, and 5) antidromic electrical stimulation of afferents. The mast cell stabilizers cromolyn and doxantrazole suppressed release of protease II and histamine when evoked by SP, CGRP, capsaicin, A23187, electrical stimulation of afferents, or compound 48/80. Neural blockade by tetrodotoxin prevented mast cell protease II release in response to antidromic electrical stimulation of mesenteric afferents. The results support a hypothesis that afferent innervation of enteric mast cells releases histamine and mast cell protease II, both of which are known to act in a diffuse paracrine manner to influence the behavior of enteric nervous system neurons and to elevate the sensitivity of spinal afferent terminals.

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.

Neurally mediated gastric mucosal damage in hypophysectomized rats

1992 ◽  
Vol 70 (8) ◽  
pp. 1109-1116 ◽  
Author(s):  
Lynn E. Hierlihy ◽  
John L. Wallace ◽  
Alastair V. Ferguson
Keyword(s):  
Electrical Stimulation ◽  
Paraventricular Nucleus ◽  
Mucosal Damage ◽  
Pituitary Hormones ◽  
Gastric Damage ◽  
Gastric Mucosal Damage ◽  
Sprague Dawley ◽  
Vagal Nerves ◽  
Scale Control ◽  
Stimulation Of

The role of the pituitary hormones in the development of neurally mediated gastric mucosal damage was examined in both normal and hypophysectomized urethane-anaesthetized male Sprague–Dawley rats. Gastric mucosal damage was elicited either by electrical stimulation of intact vagal nerves or by electrical stimulation in the paraventricular nucleus. Macroscopic damage was scored following the stimulation period and samples of the stomach were fixed for histological assessment. Damage scores were assigned based on a 0 (normal) to 3 (severe) scale. Control experiments in which the vagi were not stimulated did not result in any significant gastric damage in either normal (0.56) or sham surgery (0.14) animals, whereas hypophysectomized animals were observed to have significant damage (1.44, p < 0.05). Stimulation of the vagi in hypophysectomized animals resulted in damage that was not significantly different compared with the hypophysectomized control animals (1.25, p > 0.05). In normal animals, stimulation of vagal nerves resulted in mean damage scores of 2.00, values that were not significantly different from those observed in hypophysectomized animals (1.25, p > 0.05). Similarly, stimulation in the paraventricular nucleus of hypophysectomized animals resulted in gastric lesions (2.00) that were not significantly different from those observed in normal animals (1.91, p > 0.05). These data suggest that such neurally mediated gastric damage does not depend upon neurosecretory projections to the pituitary gland, but that the maintenance of an intact gastric mucosa under normal conditions requires the presence of pituitary hormones.Key words: vagus, paraventricular nucleus, hypophysectomy, gastric.

Suckling-induced release of cholecystokinin into plasma in the lactating rat: effects of abdominal vagotomy and lesions of central pathways concerned with milk ejection

1990 ◽  
Vol 127 (2) ◽  
pp. 257-263 ◽  
Author(s):  
A. Linden ◽  
M. Eriksson ◽  
S. Hansen ◽  
K. Uvnäs-Moberg
Keyword(s):  
Electrical Stimulation ◽  
Plasma Levels ◽  
Vagal Nerve ◽  
Milk Ejection ◽  
Vagal Nerves ◽  
Plasma Cholecystokinin ◽  
Milk Ejection Reflex ◽  
Stimulation Of

ABSTRACT Plasma levels of cholecystokinin were increased in response to suckling in lactating rats. Efferent electrical stimulation of the vagal nerve increased the concentration of cholecystokinin in plasma. Abdominal vagotomy was found to block the suckling-induced release of cholecystokinin. Furthermore, lesions to the lateral midbrain, which disrupt the oxytocin-mediated milk-ejection reflex, were shown to inhibit the increase in plasma cholecystokinin. These results show that the suckling-induced release of cholecystokinin into plasma in lactating rats is dependent upon the vagal nerves and the central neural structures concerned with milk let-down. Journal of Endocrinology (1990) 127, 257–263

scholarly journals 5 MUCOSAL MAST CELLS IN THE BABY RAT JEJUNUM

1988 ◽  
Vol 24 (3) ◽  
pp. 406-406
Author(s):  
M Varkasalo ◽  
A Fergucon ◽  
H R P Millor ◽  
A Cummins
Keyword(s):  
Mast Cells ◽  
Rat Jejunum ◽  
Mucosal Mast Cells
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