Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Immunocytochemical application of the antimuscarinic acetylcholine receptor antibody M35 to pancreas tissue revealed the target areas for the parasympathetic nervous system. Immunoreactivity in the endocrine pancreas was much higher than that in the exocrine part. Moreover, the endocrine cells at the periphery of the islets of Langerhans displayed the highest level of immunoreactivity. Based on these findings in the mantle of the islets, two types of islets have been distinguished: type-I islets with intensely stained mantle cells, and type-II islets with a much lower concentration of these cells. On average, type-I islets were larger (244.8 microns +/- 6.1 SEM) than type-II islets (121.5 microns +/- 3.8 SEM). M35-immunoreactivity was present on the majority of D cells, which were characterized by their immunoreactivity to somatostatin [of 446 D cells 356 (79.8%) were M35-immunopositive]. However, only a small proportion of the intensely stained mantle cells belonged to the D cell population. Therefore, it is concluded that the majority of the intensely stained mantle cells represent glucagon-secreting A and/or pancreatic polypeptide-secreting F cells. The intensity of M35-immunoreactivity at the periphery and central core of the islets paralleled the density of cholinergic innervation, suggesting a positive correlation between the intensity of cholinergic transmission and the number of muscarinic acetylcholine receptors at the target structures. The present study further revealed some striking parallels for the muscarinic acetylcholine receptor characteristics between the (endocrine) pancreas and the central nervous system.
 ...
PMID:Immunocytochemical localization of muscarinic acetylcholine receptors in the rat endocrine pancreas. 135 50

An impairment of cholinergic and somatostatinergic neurotransmission have been reported in dementia. Both acetylcholine and somatostatin are involved in the regulation of growth hormone (GH) secretion. The effects of GH-releasing hormone (GHRH) 1-44 on GH release have been studied before and after the pretreatment with pyridostigmine or pirenzepine in subjects with senile dementia of the Alzheimer type, multi-infarct dementia and mixed dementia. The data have been compared with those obtained in an age-matched healthy control group. The GH response to GHRH is similar in the patients and in the controls, though the peak occurrence is significantly delayed in dementia. The cholinesterase inhibitor pyridostigmine enhances significantly the GH response to GHRH in both groups. The responses obtained in demented subjects are significantly larger than those found in the controls. Pirenzepine, a muscarinic receptor blocker, inhibits the GHRH effect on GH secretion in both groups. The findings may be interpreted in terms of an underlying impairment of the hypothalamic cholinergic neurotransmission, with an acetylcholine receptor supersensitivity that becomes apparent when the cholinergic tonus is enhanced by the inhibition of cholinesterase by pyridostigmine. No significant differences, due to the type of dementia, have been observed.
 ...
PMID:Cholinergic modulation of growth hormone-releasing hormone effects on growth hormone secretion in dementia. 198 29

Pancreatic hormone release is generally thought to be regulated through adrenergic as well as muscarinic receptors. We have previously observed possible nicotinic involvement in insulin release. In the present study, we incubated isolated rat islets for 60 min with various concentrations of atropine (a muscarinic receptor blocker), alpha-bungarotoxin (alpha-Btx, a nicotinic receptor blocker), and anti-acetylcholine receptor antibody (IgG) (anti-Ach.R.Ab) obtained from a patient with myasthenia gravis. Atropine suppressed insulin release, and alpha-Btx and anti-Ach.R.Ab potentiated it; atropine did not suppress glucagon release, while alpha-Btx and anti-Ach.R.Ab raised it. None of these agents influenced somatostatin release. These observations suggest that muscarinic as well as nicotinic receptors influence insulin release, as nicotinic receptors do glucagon release. Neither nicotinic nor muscarinic receptors seem to regulate somatostatin release.
 ...
PMID:Participation of nicotinic receptor in hormone release from isolated rat islets of Langerhans. 256 21

The colocalization of acetylcholine (ACh) and neuropeptides (e.g., substance P and enkephalins) in the splanchnic nerve terminals suggests that these compounds might interact to modulate adrenal catecholamine release. Use has been made of primary monolayer and suspension cultures of bovine adrenal chromaffin cells to investigate postsynaptic receptor interactions between acetylcholine and a number of neuropeptides endogenous to the adrenal medulla and splanchnic nerve. The cells have both nicotinic and muscarinic acetylcholine receptors, but only the nicotinic receptors stimulate catecholamine release. Substance P, somatostatin, and the enkephalins all produced an inhibition of the ACh-evoked secretion of catecholamines, but their potency ranged over 100-fold. Substance P was the most potent with a mean inhibitory concentration (IC50) of 10(-6) M and Leu-enkephalin the least potent with an IC50 greater than 10(-4) M. These pharmacological effects were monitored conveniently by measuring the release of [3H]norepinephrine preloaded into the cells or alternatively, "on-line" by measuring ATP released into an incubation medium containing luciferin and firefly tail extract (luciferase). Of interest, the endogenous enkephalin heptapeptide (Met-enkephalin Arg6-Phe7) and "big" Met-enkephalin (BAM- 22P ) were some 100-fold more effective than Leu- or Met-enkephalin at inhibiting the nicotinic secretin of catecholamines, suggesting that a unique opiate receptor may be involved. Substance P had two distinct actions on the nicotinic response: (1) substance P inhibited acetylcholine-induced release of catecholamines; and (2) substance P protected against acetylcholine-induced desensitization of catecholamine release. With regard to (1), substance P inhibited the secretion of catecholamines and ATP evoked by acetylcholine or nicotine but not that evoked by K+ or veratridine, nor did substance P by itself affect secretion. Substance P appeared to interact with a regulatory site on the acetylcholine receptor - ionophore complex. Substance P receptors on chromaffin cells have similar structural requirements for activation as do substance P receptors in other substance P responsive tissues. With regard to (2), substance P (greater than 5 X 10(-6) M) completely protected against desensitization of catecholamine release produced by acetylcholine (greater than 10(-4) M) or nicotine (greater than 2.5 X 10(-6) M) with no effect on K+-induced desensitization.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Receptors and receptor modulation in cultured chromaffin cells. 620 33

The developing avian ciliary ganglion has been a particularly amenable system for the identification, isolation, and characterization of putative target-derived molecules that mediate retrograde interactions. To date a number of biochemically distinct activities that regulate neuronal survival, transmitter phenotype, and chemosensitivity of ciliary ganglion neurons have been identified. Of these, only two survival-promoting molecules have been purified to homogeneity: ciliary neurotrophic factor and a related molecule, growth-promoting activity. A somatostatin-inducing activity found in cultured choroid cells is very likely to be chick activin A. Other molecules that regulate acetylcholine and acetylcholine receptor expression comigrate on a gel filtration column at a molecular weight of 50-60 kD, but they have yet to be isolated. Once molecules that mimic retrograde influences are identified, a number of criteria must be met before their physiological significance can be established. These criteria are (1) availability of the molecule from the target at the appropriate time in development; (2) ability of the neurons to respond to the molecule at the appropriate time in development; (3) demonstration that blocking the activity or availability of the molecule is able to block the target-derived developmental change expressed in the neurons. Of the molecules that are thought to retrogradely influence ciliary neuron development, only growth-promoting activity is known to meet criteria 1 and 2, and experiments are currently underway to test whether inhibition of growth-promoting activity in vivo will exacerbate normal cell death.
 ...
PMID:Target-derived molecules that influence the development of neurons in the avian ciliary ganglion. 791 99

2-Deoxyglucose (2-DG) uptake is an index of regional glucose utilization which reflects predominantly activity in the axonal terminal of neuronal pathways. The present experiments showed that somatostatin elevated 2-DG uptake in rat cortex and hippocampus slices. Treatment with somatostatin-14 and somatostatin-28 markedly enhanced 2-DG uptake, whereas the amino-terminal fragment of somatostatin-28 did so only slightly. This effect appeared to be mediated by an interaction with somatostatin receptors because cyclo-somatostatin, a somatostatin antagonist, abolished the effect of somatostatin-14. The increase in 2-DG uptake caused by somatostatin-14 was blocked by the calcium channel antagonist, nifedipine, but not by tetrodotoxin, suggesting that the action of somatostatin does not require the initiation of impulse activity, somatostatin enhanced the KCl-induced release of acetylcholine, suggesting that a cholinergic mechanism is involved in the somatostatin-induced cellular responses. We therefore examined whether acetylcholine receptor antagonists block the somatostatin-induced increase in 2-DG uptake. Neither muscarinic nor nicotinic receptor antagonists affected the somatostatin-14-induced response. The present results suggest that somatostatin has a stimulatory effect on energy metabolism and that this effect is independent of acetylcholine receptor mechanism.
 ...
PMID:Facilitation of 2-deoxyglucose uptake in rat cortex and hippocampus slices by somatostatin is independent of cholinergic activity. 809 64

Axons of retinal ganglion cells (RGCs) carry visual information to the brain. In most vertebrates, the major synaptic target of RGCs is the optic tectum. In the chick, RGC axons form synapses in just 4 of 16 histologically recognizable laminae (the retinorecipient laminae [RRLs]), and arbors of individual RGCs are confined to a single RRL. To analyze the development and function of these parallel pathways, markers are required that selectively label them. Here, we have identified molecular markers for individual RRLs and for RGCs that project to them. Some of the markers may mediate or modulate signaling through the separate pathways: neuropeptides (substance P, neuromedin B, somatostatin-I and -II) and their receptors (substance P receptor), neurotransmitter synthetic enzymes (choline acetyltransferase) and the corresponding receptors (acetylcholine receptor beta2) and calcium-binding proteins (parvalbumin and calbindin). Other markers are adhesive proteins that could mediate selective connectivity of RGC subsets within specific RRLs (cadherin-7, cadherin-11, reelin and neuropilin-1). We further show that RGC subsets whose axons project to specific RRLs are heterogeneous with respect to the retinal sublaminae within which their dendrites arborize. Our results define laminar-specified circuits from retina to brain and support a model in which RGCs transmit information from multiple sources to single central laminae, where it can be integrated.
 ...
PMID:Labeled lines in the retinotectal system: markers for retinorecipient sublaminae and the retinal ganglion cell subsets that innervate them. 1697 78

Consumption of coffee beverages has been reported to cause gastric irritation in some consumers as a result of increased gastric acid secretion. In the complex mechanisms of gastric acid secretion, the activity and expression of the H+,K+-ATPase is regulated by transmitters, such as histamine, acetylcholine, gastrin, somatostatin, and their corresponding receptors. Here, we report the effect of three coffee constituents, chlorogenic acid, caffeine, and N-methyl pyridinium ions, on the expression of the histamine receptor H2, the acetylcholine receptor M3, the gastrin receptor, the somatostatin receptor, and the H+,K+-ATPase. Human gastric cancer cells were exposed to chlorogenic acid, caffeine, or N-methyl pyridinium in their coffee brew-representative concentrations as well as to physiological stimulators of gastric acid secretion. Gene expression levels of receptor proteins and those of the H+,K+-ATPase were measured at different time points by real-time PCR. Expression of prosecretory receptors significantly increased between one and one-half to twofold after treatment with chlorogenic acid or caffeine compared to control cells at the same time point. Chlorogenic acid and caffeine also increased the H+,K+-ATPase gene expression twofold higher compared to control cells. In contrast, N-methyl pyridinium downregulated the expression of the prosecretory gastrin receptor significantly, by -27%. In conclusion, chlorogenic acid, caffeine, and N-methyl pyridinium impair the expression of gastric acid secretion-related proteins in a time-dependent manner. Future work will be aimed at the elucidation of the cooperative interplay of individual components using recombinates of single coffee constituents.
 ...
PMID:Time-dependent component-specific regulation of gastric acid secretion-related proteins by roasted coffee constituents. 1844 37

The role of somatostatin receptors in the nucleus accumbens shell in rat turning behaviour was studied. Unilateral injection of neither the somatostatin receptor agonist somatostatin (1.0 microg) nor the somatostatin receptor antagonist cyclosomatostatin (100.0 ng) into the nucleus accumbens shell elicited turning behaviour. Unilateral injection of a mixture of dopamine D(1) ((+/-)-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine-7,8-diol, SKF 38393) and D(2/3) (quinpirole) receptor agonists into the nucleus accumbens shell has been found to elicit contraversive pivoting. Somatostatin (0.5 and 1.0 microg) dose-dependently potentiated the contraversive pivoting induced by a mixture of SKF 38393 (1.0 microg) and quinpirole (10.0 microg) injected into the nucleus accumbens shell. This potentiating effect of somatostatin (1.0 microg) on the dopaminergic pivoting was dose-dependently inhibited by cyclosomatostatin (10.0 and 100.0 ng) injected into the nucleus accumbens shell. Unilateral injection of acetylcholine receptor agonist carbachol into the nucleus accumbens shell has been found to elicit contraversive circling. Neither somatostatin (1.0 ?g) nor cyclosomatostatin (100.0 ng) significantly affected the contraversive circling induced by carbachol (5.0 microg) injected into the nucleus accumbens shell. These results suggest that somatostatin receptors in the nucleus accumbens shell play a modulatory role in rat dopaminergic pivoting, but not in rat cholinergic circling.
 ...
PMID:Somatostatin receptors in the nucleus accumbens modulate dopamine-dependent but not acetylcholine-dependent turning behaviour of rats. 1935 81

We investigated the roles of muscarinic (M) acetylcholine receptor subtype in the cholinergic stimulation of duodenal HCO3(-) secretion using knockout (KO) mice. Wild-type and M1-M5 KO C57BL/6J mice were used. The duodenal mucosa was mounted on an Ussing chamber, and HCO3(-) secretion was measured at pH 7.0 using a pH-stat method in vitro. Carbachol (CCh) or other agents were added to the serosal side. CCh dose-dependently stimulated HCO3(-) secretion in wild-type mice, and this effect was completely inhibited in the presence of atropine. The HCO3(-) response to CCh in wild-type mice was also inhibited by pirenzepine (M1 antagonist), 4DAMP (M3 antagonist), and tropicamide (M4 antagonist), but not by methoctramine (M2 antagonist). CCh stimulated HCO3(-) secretion in M2 and M5 KO animals as effectively as in WT mice; however, this stimulatory effect was significantly attenuated in M1, M3, and M4 KO mice. The decrease observed in the CCh-stimulated HCO3(-) response in M4 KO mice was reversed by the co-application of CYN154806, a somatostatin receptor type 2 (SST2) antagonist. Octreotide (a somatostatin analogue) decreased the basal and CCh-stimulated secretion of HCO3(-) in wild-type mice. The co-localized expression of somatostatin and M4 receptors was confirmed immunohistologically in the duodenum. We concluded that the duodenal HCO3(-) response to CCh was directly mediated by M1/M3 receptors and indirectly modified by M4 receptors. The activation of M4 receptors was assumed to inhibit the release of somatostatin from D cells and potentiate the HCO3(-) response by removing the negative influence of somatostatin via the activation of SST2 receptors.
...
PMID:Muscarinic acetylcholine receptor subtype 4 is essential for cholinergic stimulation of duodenal bicarbonate secretion in mice - relationship to D cell/somatostatin. 2608 21


1 2 Next >>