Distribution and Morphology of Somatostatin Cells

To determine whether mesenchyme plays a part in the differentiation of gut endocrine cells, proventricular endoderm from 4- to 5-day chick or quail embryos was associated with mesenchyme from the dorsal pancreatic bud of chick embryos of the same age. The combinations were grown on the chorioallantoic membranes of host chick embryos until they reached a total incubation age of 21 days. Proventricular or pancreatic endoderm of the appropriate age and species reassociated with its own mesenchyme provided the controls. Morphogenesis in the experimental grafts corresponded closely to that in proventricular controls, i.e. the pancreatic mesenchyme supported the development of proventricular glands from proventricular endoderm. Insulin, glucagon and somatostatin cells and cells with pancreatic polypeptide-like immunoreactivity differentiated in the pancreatic controls. The latter three endocrine cell types, together with neurotensin and bombesin/gastrin-releasing polypeptide (GRP) cells, developed in proventricular controls and experimental grafts. The proportions of the major types common to proventriculus and pancreas (somatostatin and glucagon cells) were in general similar when experimental grafts were compared with proventricular controls but different when experimental and pancreatic control grafts were compared. Hence pancreatic mesenchyme did not materially affect the proportions of these three cell types in experimental grafts, induced no specific pancreatic (insulin) cell type and allowed the differentiation of the characteristic proventricular endocrine cell types, neurotensin and bombesin/GRP cells. However, an important finding was a significant reduction in the proportion of bombesin/GRP cells, attributable in part to a decrease in their number and in part to an increase in the numbers of endocrine cells of the other types. This indicates that mesenchyme may well play a part in determining the regional specificity of populations of gut endocrine cells.

Download Full-text

Lansoprazole and Omeprazole Have Similar Effects on Plasma Gastrin Levels, Enterochromaffin-Like Cells, Gastrin Cells and Somatostatin Cells in the Rat Stomach

Digestion ◽

10.1159/000200887 ◽

1992 ◽

Vol 51 (3) ◽

pp. 125-132 ◽

Cited By ~ 25

Author(s):

Hong Lee ◽

Rolf Håkanson ◽

Agneia Karlsson ◽

Hillevi Mattsson ◽

Frank Sundler

Keyword(s):

Rat Stomach ◽

Plasma Gastrin ◽

Gastrin Cells ◽

Somatostatin Cells

Download Full-text

Somatostatin cells regulate sensory response fidelity via subtractive inhibition in olfactory cortex

Nature Neuroscience ◽

10.1038/nn.3971 ◽

2015 ◽

Vol 18 (4) ◽

pp. 531-535 ◽

Cited By ~ 36

Author(s):

James F Sturgill ◽

Jeffry S Isaacson

Keyword(s):

Olfactory Cortex ◽

Sensory Response ◽

Somatostatin Cells

Download Full-text

Ablation of somatostatin cells leads to impaired pancreatic islet function and neonatal death in rodents

Cell Death and Disease ◽

10.1038/s41419-018-0741-4 ◽

2018 ◽

Vol 9 (6) ◽

Cited By ~ 8

Author(s):

Na Li ◽

Zhao Yang ◽

Qing Li ◽

Zhen Yu ◽

Xu Chen ◽

...

Keyword(s):

Pancreatic Islet ◽

Neonatal Death ◽

Islet Function ◽

Somatostatin Cells

Download Full-text

Septal Signaling Suppresses Seizures Through Stimulating Somatostatin Cells

Epilepsy Currents ◽

10.1177/1535759720949240 ◽

2020 ◽

Vol 20 (5) ◽

pp. 297-299

Author(s):

Patrick A. Forcelli

Keyword(s):

Somatostatin Cells

[Box: see text]

Download Full-text

Phorbol esters stimulate somatostatin release from cultured cells

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1986.250.5.g686 ◽

1986 ◽

Vol 250 (5) ◽

pp. G686-G690 ◽

Cited By ~ 2

Author(s):

K. Sugano ◽

J. Park ◽

A. Soll ◽

T. Yamada

Keyword(s):

Protein Kinase C ◽

Protein Kinase ◽

Phorbol Esters ◽

Cultured Cells ◽

Cyclic Adenosine Monophosphate ◽

Adenosine Monophosphate ◽

Ionophore A23187 ◽

Muscarinic Agonists ◽

Kinase C ◽

Somatostatin Cells

Recent studies suggest that 12-O-tetradecanoylphorbol 13-acetate (TPA), one of a family of phorbol esters that are known tumor promoters, can activate intracellular Ca2+, phospholipid-dependent protein kinase (protein kinase C) directly. To examine the possible involvement of protein kinase C-mediated mechanisms in regulating gastric somatostatin release, we studied the effects of TPA on isolated enriched canine gastric somatostatin cells in short-term culture. TPA markedly stimulated somatostatin release such that nearly 10% of total cellular content of somatostatin was released into media within 2 h of incubation. Among the phorbol compounds tested, TPA was the most potent, with half-maximum effective dose (ED50) obtained at a dose of 5 X 10(-9) M. Phorbol 12,13-dibutyrate (PDBu) also stimulated somatostatin release but with only 5% of the potency of TPA, whereas phorbol compounds with no biological activity in other systems failed to stimulate somatostatin release. In the absence of extracellular Ca2+, the effects of TPA were significantly attenuated. In contrast, stimulation of somatostatin release by forskolin (10(-4) M) was not affected by Ca2+ deprivation but was potentiated by TPA. No such potentiation was observed when TPA was combined with the Ca2+ ionophore A23187. Carbamylcholine (10(-5) M), which inhibits the stimulatory actions of beta-adrenergic agonists or dibutyryl cyclic adenosine monophosphate on somatostatin cells, also inhibited TPA-induced somatostatin release. These data suggest the presence of dual stimulatory mechanisms for gut somatostatin release, both of which are susceptible to inhibition by muscarinic agonists.

Download Full-text

Functionally distinct muscarinic receptors on gastric somatostatin cells

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1990.258.6.g982 ◽

1990 ◽

Vol 258 (6) ◽

pp. G982-G987 ◽

Cited By ~ 5

Author(s):

M. L. Schubert ◽

J. Hightower

Keyword(s):

Muscarinic Receptors ◽

Pertussis Toxin ◽

Inhibitory Effect ◽

Tetraacetic Acid ◽

Muscarinic Agonists ◽

Rat Stomach ◽

Dominant Effect ◽

Somatostatin Secretion ◽

Somatostatin Cells ◽

Stimulation Of

The present study was designed to examine the mode of action of muscarinic agonists on somatostatin secretion in intact gastric tissues, i.e., mucosal segments from the fundus and antrum of rat and the isolated luminally perfused mouse stomach. Methacholine caused similar decreases in somatostatin secretion in segments from the fundus (35 +/- 3%; P less than 0.001) and antrum (35 +/- 2%; P less than 0.001) of rat stomach, and in whole mouse stomach (43 +/- 3%; P less than 0.001). The decrease was the net effect of a dominant inhibition and a lesser stimulation of somatostatin secretion. Pretreatment with the permeant derivative of the acetomethoxy ester form of the calcium chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA/AM, 15 microM) caused a further decrease in methacholine-induced somatostatin secretion, implying that a stimulatory component existed that was mediated by intracellular calcium. Pretreatment with pertussis toxin (125 ng/ml) for 60 min converted the decrease in somatostatin secretion to an increase above basal levels. The increase induced by pretreatment with pertussis toxin was abolished by additional pretreatment with BAPTA/AM. Procaine (5 mM), which blocks release of calcium from intracellular stores, produced an effect on somatostatin secretion similar to that of BAPTA/AM. The results indicate that 1) methacholine exerts dual inhibitory and stimulatory effects on somatostatin cells of rat and mouse stomach, 2) the dominant effect is inhibitory and sensitive to pertussis toxin, and 3) a concurrent stimulatory effect, mediated by calcium, is unmasked after blockade of the inhibitory effect with pertussis toxin.

Download Full-text