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

The topography of the peptidergic neuronal subpopulations in the guinea pig celiac-superior mesenteric ganglion was studied analyzing the distribution of immunoreactivity to neuropeptide Y (NPY), somatostatin (SOM), and vasoactive intestinal polypeptide (VIP)/polypeptide HI (PHI). For comparison, the ganglion was also studied using antisera against the 2 catecholamine-synthesizing enzymes tyrosine hydroxylase (TH) and dopamine beta-hydroxylase (DBH). Approximately 65% of the neuronal cell bodies contained NPY-like immunoreactivity (NPY-LI), whereas 25% of the principal ganglion cells contained SOM-like immunoreactivity (SOM-LI). Though occasional cells were found to contain both NPY-LI and SOM-LI, these peptides had a complementary distribution in the ganglion, with NPY cells in the celiac poles and SOM cells in the superior mesenteric pole. The vast majority of both the NPY- and SOM-positive cells also contained TH-like immunoreactivity (TH-LI), confirming their catecholaminergic, presumably noradrenergic, nature. Some noradrenergic neurons seemed to lack NPY- and SOM-LI. Small numbers of VIP/PHI-containing cell bodies were found in areas where the NPY-immunoreactive neurons predominated. Many of the VIP/PHI-positive cells contained NPY-LI and occasionally also TH-LI. The immunohistochemical markers were also observed in fibers. Thus, a comparatively weak NPY-LI was seen in smooth fibers, probably representing axons and axon bundles. SOM-LI was seen in a similar type of fiber but also in more strongly fluorescent fibers with a varicose appearance. The latter fibers were observed only in the SOM-dominated part of the ganglion, often surrounding the ganglion cells. Varicose fibers with a similar distribution containing DBH-like immunoreactivity (DBH-LI) were also seen. In addition, DBH- and TH-LI were seen in smooth axonlike processes. VIP-positive fibers exhibited a very dense fiber network, almost exclusively related to the SOM cell-dominated part of the ganglion. The projection of the postganglionic sympathetic neurons was studied with special reference to the pylorus using a combination of retrograde axonal tracing and indirect immunofluorescence techniques. Seventy-two hours after injection of the fluorescent tracer Fast Blue into the pyloric sphincter, labeled neurons were found in the ganglion. By comparing the Fast Blue-labeled cells with the immunoreactive cell bodies, neurons containing both dye and NPY- or SOM-LI were observed. In elution-restaining experiments, it was established that the majority of these cells were also immunoreactive to TH, indicating that they produce noradrenaline.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Topography of NPY-, somatostatin-, and VIP-immunoreactive, neuronal subpopulations in the guinea pig celiac-superior mesenteric ganglion and their projection to the pylorus. 287 37

The evidence for deficiencies in neurotransmitters in Alzheimer's disease is reviewed. Major losses occur in the subcortical afferent projection systems based on acetylcholine, noradrenaline and serotonin. Within the cortex, somatostatin containing neurones and the large pyramidal cells, presumed to use glutamate/aspartate as transmitters, are the most severely damaged cells. The anatomical distribution of cell loss is explainable if the primary site of damage lies within the cortex; nerve cells are damaged by virtue of their presence within or their connections to this region. The senile plaque may represent the site of this damage and neurofibrillary tangle formation and accumulation may lead to cell death. In patients with Down's syndrome who live past 40 years, changes in transmitters apparently identical to those in Alzheimer's disease occur. The dementia of Parkinson's disease appears related to damage to cholinergic, noradrenergic and dopaminergic systems and may reflect a failure of these subcortical regions to sufficiently "activate" an otherwise undamaged cortex.
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PMID:Neurotransmitter deficits in Alzheimer's disease and in other dementing disorders. 287 73

Noradrenaline (NA) and somatostatin (SOM) stimulate intestinal water and ion absorption and are found in mucosal nerve fibres and nerve terminals in submucous ganglia of the guinea-pig small intestine. As the main projection of submucous neurons is to the mucosa, NA and SOM might alter mucosal transport either by a direct effect on the epithelium or indirectly, by affecting submucous neurons. In this study these two possible sites of action of NA and SOM have been investigated in mucosa-submucosa preparations of guinea-pig ileum. In addition, the actions of NA and SOM on the secretory responses caused by stimulation of different populations of submucous neurons have been studied. The stimulants of secretion used were a nicotinic agonist, 1,1-dimethyl-4-phenylpiperazinium (DMPP, 10(-5) M), 5-hydroxytryptamine (5-HT, 10(-7) M) and electrical field stimulation (EFS), which activate cholinergic, noncholinergic and mixed populations of submucous secretomotor neurons, respectively. Segments of intestine were dissected free of external muscle and myenteric plexus and mounted in Ussing chambers. Short-circuit current (Isc) was measured as an indication of net active ion transport across the tissue. NA (greater than or equal to 10(-8) M) and SOM (greater than 10(-10) M) each caused a decrease in Isc, indicating a net increase in ion absorption. The NA response was abolished and the magnitude of the SOM response was reduced to 20% by tetrodotoxin (10(-7) M). DMPP, 5-HT and EFS each stimulated nerves that increased Isc and each of these responses was significantly diminished by NA and SOM.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of noradrenaline and somatostatin on basal and stimulated mucosal ion transport in the guinea-pig small intestine. 287 1

A [K+]-related, Ca2+-dependent efflux of immunoreactive somatostatin (IRS) from superfused slices of rat cerebral cortex has been observed; this release paralleled the release of both [14C]noradrenaline and [14C]GABA. However IRS release in this preparation was not stimulated by the muscarinic agonist carbachol at low (10 microM) or high (500 microM) concentrations. Furthermore, 100 or 500 microM carbachol did not affect the IRS efflux from rat cortex slices incubated in the presence of 12, 25 or 53 mM K+.
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PMID:Failure of carbachol to influence the release of somatostatin from slices of rat cerebral cortex. 287 3

Gillichthys urotensin II (GUII; 1.5-150 nmol kg-1) reduced blood pressure in anesthetized rats, diastolic pressure being reduced to a greater extent than systolic. The effect was slow in onset (peak at 4-5 min) and longlasting (up to 60 min), and was accompanied by a reflex tachycardia. The hypotension was not blocked by propranolol or by mepyramine. In pithed rats, GUII (150 nmol kg-1) reduced the pressor responses to sympathetic nerve stimulation, noradrenaline, and Arg-vasopressin. Somatostatin (150 nmol kg-1) had no effect on the sympathetic pressor response but reduced heart rate. It is concluded that GUII is a vasodilator in the rat, an action not shared with somatostatin.
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PMID:Cardiovascular effects of urotensin II in anesthetized and pithed rats. 287 65

Inotropic responses to calcitonin gene-related peptide (alpha-CGRP), substance P, neurokinin A, capsaicin, neuropeptide Y, vasoactive intestinal polypeptide (VIP) and somatostatin (Som, 14 and 28 were analysed using the isolated, electrically driven auricle of the human right atrium. alpha-CGRP and VIP stimulated atrial contractility concentration dependently. alpha-CGRP was about 10-fold more potent than noradrenaline (NA) as an inotropic agent. Phentolamine plus metoprolol decreased the atrial response to NA significantly while the alpha-CGRP effect remained unchanged. Som did not influence the basal contractility of the atria, which, however, was inhibited by acetylcholine (ACh). ACh, Som 14 and Som 28 inhibited the NA-induced stimulation of atrial contractility, whereby Som 28 was more potent than Som 14. The inhibitory effects of ACh were completely blocked by atropine which did not influence the response to Som. Capsaicin, substance P, neurokinin A, neuropeptide Y (NPY) and the NPY fragments 1-19 and 26-36 did not induce any changes in contractility of the electrically driven human atrium. The present results suggest that some of the recently discovered neuropeptides (alpha-CGRP, VIP and Som) could be of importance in the regulation of cardiac contractility in man.
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PMID:Inotropic effects of calcitonin gene-related peptide, vasoactive intestinal polypeptide and somatostatin on the human right atrium in vitro. 288 95

The present study aimed at evaluating the effect of human beta-endorphin on pancreatic hormone levels and on glucose metabolism in normal subjects. Infusion of 143 nmol/h beta-endorphin in 7 subjects caused a significant rise in plasma glucose concentrations (+ 1.7 +/- 0.3 mmol/l) which was preceded by a significant increase in peripheral plasma glucagon levels (+ 44 +/- 13 ng/l). No changes occurred in the plasma concentrations of insulin and catecholamines (adrenaline and noradrenaline). The influence of beta-endorphin per se on glucose homeostasis was studied in 7 other subjects using the euglycaemic clamp technique in which the endocrine pancreatic function was fixed at its basal level with somatostatin together with replacement of basal insulin and glucagon by the exogenous infusion of these hormones. In this new metabolic conditions, beta-endorphin failed to have significant influences on the various parameters of tracer-estimated glucose metabolism (production, utilization, and clearance) and on the plasma levels of the gluconeogenic precursors (glycerol and alanine). Moreover, the levels of pancreatic and counterregulatory hormones (cortisol and catecholamines) were not different between beta-endorphin and control studies. We conclude that the naturally occurring opioid peptide beta-endorphin produced an hyperglycaemic effect in man which appears to be mediated by glucagon. The opioid seems to have no direct effect on glucose metabolism. These results suggest that the metabolic effects of beta-endorphin in normal man are secondary to its impact on pancreatic hormone secretion and not a consequence of a direct modulation of glucose metabolism.
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PMID:Primary role of glucagon release in the effect of beta-endorphin on glucose homeostasis in normal man. 288 94

The localization of somatostatin-like immunoreactivity (SOM-LI) was examined in human lumbar sympathetic ganglia using the peroxidase-antiperoxidase method. Few of the principal neurons showed immunolabelling for somatostatin and sparse networks of nerve terminals were unevenly associated with ganglion cells. Using light microscopy, the most intense SOM-LI was seen in the perinuclear zone of the neurons. Electron-microscopically, the staining was localized on the membranes of the Golgi apparatuses. In the nerve terminals, SOM-LI was seen inside the small vesicles (40-60 nm diameter). All neurons with SOM-LI were also found to be tyrosine-hydroxylase immunoreactive when examined with a double-staining technique. These results provide evidence that somatostatin and noradrenaline co-exist in human sympathetic neurons.
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PMID:Somatostatin-like immunoreactivity in human sympathetic ganglia. 288 89

The effect of the artificial sweetener Acesulfame K on insulin release in vitro was investigated. Pancreatic islets were obtained from Male Wistar rats. Acesulfame K produced a significant increase in insulin release from incubated islets. This effect was dose- and glucose-dependent. When islets were incubated with different amounts of Acesulfame K (2.5, 7.5 and 15 mM) and 15 mM glucose in the media for one hour, insulin concentrations were 140.2 +/- 21.1, 246.7 +/- 32.4 and 313.9 +/- 37.7 microU/ml, respectively. When 15 mM Acesulfame K was added to a media containing 0, 2.5, 5, 10 and 15 mM glucose, insulin release from incubated islets after 60 min were 25.6 +/- 6.4, 65.4 +/- 12.1, 109.0 +/- 10.0, 229.6 +/- 28.0 and 313.9 +/- 37.7 microU/ml. Incubating islets in the media containing arginine or acetylcholine increased insulin release significantly. However, when Acesulfame K was added to the media containing either arginine or acetylcholine, no further potentiating effect could be detected. The effect of Acesulfame K on insulin secretion was decreased by noradrenaline. However, the addition of naloxone, atropine and propranolol had no significant effect. Somatostatin inhibited insulin release from isolated pancreatic islets, but did not antagonize the action of Acesulfame K. When 2.5 mM Acesulfame K was added to a medium containing somatostatin, the inhibitory effect of somatostatin was totally neutralized. In a perifusion system, Acesulfame K stimulated both phases of insulin secretion. In conclusion, Acesulfame K acts directly on the pancreatic islets and potentiates glucose-induced insulin release.
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PMID:The effect of artificial sweetener on insulin secretion. II. Stimulation of insulin release from isolated rat islets by Acesulfame K (in vitro experiments). 288 3

Synaptic organization of the intermediolateral nucleus of the guinea pig thoracic spinal cord was examined with particular focus on monoamine- and peptide-containing nerve terminals. Axon varicosities having flat synaptic vesicles constituted 17% of all axons in the nucleus and formed exclusively symmetric synapses. Enkephalin-, substance P-, somatostatin-, 5-hydroxytryptamine-, and catecholamine-immunoreactive nerve terminals were densely distributed, while neurotensin, vasoactive intestinal polypeptide-, oxytocin-, and cholecystokinin-8-immunoreactive nerves were sparse in the nucleus. Coexistence of 5-hydroxytryptamine and enkephalin was demonstrated, and coexistence of somatostatin and enkephalin as well as somatostatin and 5-hydroxytryptamine in the same axons was also shown by serial semithin sections. Catecholamine axons labelled by 5-hydroxydopamine formed axodendritic and axosomatic synapses and made direct synaptic contacts on the preganglionic sympathetic neurons identified by retrograde transport of horseradish peroxidase. Direct synaptic contacts from enkephalin- and substance P-immunoreactive axons to preganglionic sympathetic neurons were also revealed. Enkephalin-, substance P-, and 5-hydroxytryptamine-immunoreactive axons formed axodendritic and axosomatic synapses. Catecholamine axon varicosities constituted 19% of all axon varicosities in the nucleus and 30% of them showed synaptic specializations in a sectional plane. Axon varicosities immunoreactive to enkephalin, 5-hydroxytryptamine, and substance P constituted approximately 35, 19, and 13% of all axon varicosities, respectively, while those with synaptic contacts made up 27, 30, and 26%, respectively, in a sectional plane. Enkephalin-, 5-hydroxytryptamine-, and noradrenaline-immunoreactive axons showed mainly symmetric synaptic contacts.
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PMID:Synaptic structure of the monoamine and peptide nerve terminals in the intermediolateral nucleus of the guinea pig thoracic spinal cord. 288 97


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