Selective ligand-induced intracellular calcium changes in a population of rat isolated gastric endocrine cells

Zeng, Ningxin; Jh, Walsh; Tai, Kang; Helander, KG; Helander, Herbert F.; Sachs, George

doi:10.1053/gast.1996.v110.pm8964409

Cited by 43 publications

(37 citation statements)

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“…Nevertheless, few (if any) inconsistencies have been found between the results of video-imaging and release measurements in this particular preparation. In this preparation, there are less than 2% D cells, and the addition of somatostatin antibody has not affected either calcium signaling or histamine release in response to a variety of agonists (3,4).…”

Section: Introductionmentioning

confidence: 95%

“…This has been done by measurement of calcium signals under superfusion conditions using video microscopy, and by histamine or pancreostatin release by radioimmunoassay under static conditions (3)(4)(5). When histamine release is measured in a static system, cross-talk is a problem.…”

Section: Introductionmentioning

confidence: 99%

“…Carbachol stimulation of histamine release has not been observed. The ECL cell, if it plays a role in the neural pathway after the cephalic phase of secretion, is not responsive to the release of acetylcholine from cholinergic nerve fibers (4,5). On the other hand, about 60% of centrally stimulated acid secretion in the rat is blocked by histamine-2 antagonism (6), suggesting that a neural mediator of ECL cell function must be present to explain this effect of histamine-2 antagonists.…”

Section: Introductionmentioning

confidence: 99%

“…Stimulation of acid secretion was observed in these experiments; hence PACAP is apparently able to stimulate ECL cells, as well as D cells, in vivo. With cholinergic stimulation, there is also inhibition of D-cell function (4). The outcome of neural release of PACAP is probably determined by a balance between activation and inhibition of the regulatory pathways of acid secretion, depending on when and where PACAP and acetylcholine are released from gastric nerves.…”

Section: Introductionmentioning

confidence: 99%

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PACAP type I receptor activation regulates ECL cells and gastric acid secretion

Zeng¹,

Athmann²,

Tai³

et al. 1999

J. Clin. Invest.

116

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The regulation of acid secretion has been divided into cephalic and peripheral (gastric and intestinal) phases (1). The cephalic phase of gastric acid secretion originates in the central nervous system and impacts the hypothalamus; signals travel via the vagus nerve to the myenteric plexuses of the gastric mucosa. In the succeeding neural network, a variety of secondary neurons signal the gastric fundic and antral epithelia to influence gastric acid secretion by either primary or secondary action, namely, direct effects on parietal cells or gastric epithelial endocrine cells. The peripheral phase of acid secretion regulation involves local signaling within a variety of endocrine cells, transmitting regulatory information to the secretory cells of the gastric mucosa; the peripheral phase is more limited than the cephalic phase in terms of the possible mediators involved (2). Studies of isolated gastric endocrine cells have proved useful in defining the interactions of various signals in the regulation of gastric acid secretion, but such studies must be placed in context when considering their physiological implications. The isolated rabbit gastric gland is a more integrated model than that provided by isolated cells.With the isolation and purification (to between 85% and 95%) of functional enterochromaffin-like (ECL) cells from the rat gastric mucosa, a variety of receptors has been defined on this cell type. This has been done by measurement of calcium signals under superfusion conditions using video microscopy, and by histamine or pancreostatin release by radioimmunoassay under static conditions (3-5). When histamine release is measured in a static system, cross-talk is a problem. Superfusion of isolated, enriched ECL cells while measuring responses of intracellular calcium [Ca 2+ ] i eliminates cross-talk between possible contaminating gastric endocrine cells. Nevertheless, few (if any) inconsistencies have been found between the results of video-imaging and release measurements in this particular preparation. In this preparation, there are less than 2% D cells, and the addition of somatostatin antibody has not affected either calcium signaling or histamine release in response to a variety of agonists (3, 4).Histamine, released from ECL cells, is the most important direct stimulant of acid secretion, as shown by the broad efficacy of histamine-2 receptor antagonists as full inhibitors of gastrin and partial inhibitors of vagally stimulated acid secretion (6). The involvement of ECL cells in mediation of the cephalic (neural) phase of gastric acid secretion has been less clear. The atropine sensitivity of cephalic stimulation of acid secretion pointed

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Section: Introductionmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

PACAP type I receptor activation regulates ECL cells and gastric acid secretion

Zeng¹,

Athmann²,

Tai³

et al. 1999

J. Clin. Invest.

116

View full text Add to dashboard Cite

show abstract

“…However, cultured ECL cells have responded poorly to the M 1 agonist carbachol, raising the possibility that the effect of ACh is indirect, and precipitating a 10-year search for a suspected neural mediator. Pituitary adenylate cyclase-activating polypeptide (PACAP) has become an increasingly likely candidate since its recent identification in gastric enteric neurons (6) and the discovery of its ability to stimulate histamine secretion (7,8) and proliferation by ECL cells in culture (9). However, peripheral injection of PACAP has been shown to inhibit gastrin-stimulated acid secretion in vivo (10).…”

Section: Commentarymentioning

confidence: 99%