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)

Two distinct neuropeptide-related phenotypes are found in avian paravertebral sympathetic ganglia, corresponding to somatostatin- (SS) and vasoactive intestinal polypeptide- (VIP) expressing cells. We have detected the same cell phenotypes in cultures of embryonic quail sympathetic ganglia and have used this system to study the modulation of their expression by the environment. The cell phenotypes were identified using immunocytochemistry and induced catecholamine fluorescence and quantitative data were obtained by radioimmunoassay. Dissociation of the ganglia caused a profound increase in the expression of VIP but had no effect on SS levels. Addition of corticosterone (10(-6) M) increased the expression of SS without modifying VIP levels. In contrast, depolarization of the cells induced changes in levels of both neuropeptides. The modulation of VIP correlates with the modulation of cholinergic properties. The regulation of neuropeptide expression in the avian system shows both similarities and differences to what has been found in the mammalian system.
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PMID:Modulation of neuropeptide expression in avian embryonic sympathetic cultures. 168 May 80

Several neuropeptides known to alter gastrointestinal motility are present in milk. We investigated the effect of gastric administration of neurotensin, bombesin, somatostatin, and vasoactive intestinal polypeptide on gastrointestinal motility in suckling rats. We gavage fed 7- to 10-day-old rats with a meal consisting of 10 microliters/g of body weight of 0.9% NaCl with 51Cr tracer and one of the peptides (0, 0.1, 10, and 1,000 ng/ml). We estimated the rates of gastric emptying and the small intestinal transit from the distribution of the radioactivity in the gut. Approximately one-half of the counts emptied from the stomach in 15 min. Both gastric emptying and small intestinal transit were time dependent and were accelerated by metoclopramide and inhibited by butylscopolamine. Neurotensin 1 micrograms/ml accelerated the gastric emptying by 35% (p less than 0.02). Small intestinal transit was also accelerated (p less than 0.05). The other neuropeptides had no effect on gastric emptying and small intestinal transit. Neurotensin did not change either the gastric emptying or small intestinal transit in weaned rats, 40-50 days old, studied in the same manner. These data suggest that the intraluminal administration of neurotensin may increase gastrointestinal motility in suckling animals.
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PMID:Oral neurotensin increases gastrointestinal transit in suckling rats. 168 Oct 45

The identification of pancreastatin in pancreatic extracts prompted the investigation of its effects on islet cell function. However, in most of the investigations to date, pig pancreastatin was tested in heterologous species. Since there is great interspecies variability in the amino acid sequence of pancreastatin, we have investigated the influence of rat pancreastatin on insulin, glucagon and somatostatin secretion in a homologous animal model, namely the perfused rat pancreas. During 5.5 mM glucose infusion, pancreastatin (40 nM) inhibited insulin secretion (ca. 40%, P less than 0.025) as well as the insulin responses to 10 mM arginine (ca. 50%, P less than 0.025) and to 1 nM vasoactive intestinal polypeptide (ca. 50%; P less than 0.05). Pancreastatin failed to significantly modify glucagon or somatostatin release under any of the above experimental conditions. In addition, a lower pancreastatin concentration (15.7 nM) markedly suppressed the insulin release evoked by 11 mM glucose (ca. 85%, P less than 0.05). Our present observations reinforce the concept that pancreastatin is an effective inhibitor of insulin secretion, influencing the B-cell function directly and not through an A-cell or D-cell paracrine effect.
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PMID:Homologous pancreastatin inhibits insulin secretion without affecting glucagon and somatostatin release in the perfused rat pancreas. 168 69

The concentrations of somatostatin (SRIF), vasoactive intestinal polypeptide (VIP), beta-endorphin (beta-EP), adrenocorticotropin (ACTH) and corticotropin-releasing factor (CRF) immunoreactivity were measured in cerebrospinal fluid (CSF) of patients with Alzheimer's disease (AD), patients with Parkinson's disease (PD) and controls. In order to study the mechanisms that regulate peptide levels in CSF and peptide interactions, correlations between CSF peptides were determined. Within all patient groups a number of significant correlations were shown to exist between CSF peptides. The correlations were apparently not coincidental, since there was no such relation between the concentrations of CSF peptides and CSF protein content. Neither age, sex, severity of dementia nor the presence of extrapyramidal signs could explain the number of significant correlations. These results indicate, that the correlations found between CSF peptides may be due to common regulatory mechanisms or general physiological behaviour of peptides in the CSF.
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PMID:A correlation study of CSF neuropeptides in Alzheimer's and Parkinson's disease. 168 48

Although it seems highly likely that mammalian isocortex evolved from a structure resembling reptilian telencephalic cortex, it has been uncertain if this occurred by the laminar differentiation of three-layered reptilian cortex into six-layered mammalian isocortex without the addition of new cell types or by laminar differentiation with the addition of new cell types. To distinguish between these two possibilities, immunohistochemical techniques were used to study turtles to see if the same major neuronal cell types, as defined by neurotransmitter or neuropeptide content, present in mammalian isocortex are also present in the specific part of reptilian cortex thought to be the forerunner of at least parts of isocortex, namely the dorsal cortex. Neurons containing the following substances are the major transmitter-specific types of neurons known to be present in mammalian isocortex: cholecystokinin-8 (CCK8), vasoactive intestinal polypeptide (VIP), acetylcholine, substance P (SP), neuropeptide Y (NPY), somatostatin (SS), LANT6, enkephalin, GABA and glutamate (GLUT). In turtles, only those of the above substances that are found in large numbers of neurons in layers V-VI in mammalian isocortex, irrespective of whether they are also present in layers II-IV (i.e. SP, NPY, SS, LANT6, GABA and GLUT), were present in neurons in dorsal cortex. The neurons containing these substances in dorsal cortex in turtles were generally highly similar in morphology to their counterparts in mammalian isocortex. In contrast, neurons labeled for CCK8, VIP or acetylcholine, which are mainly found in neurons of layers II-IV of mammalian isocortex, were absent or extremely rare in dorsal cortex. The absence or paucity of neurons labeled for these latter substances in dorsal cortex in turtles did not reflect an overall staining failure of the antisera used since the same antisera yielded excellent labeling of neurons, fibers and terminals in many other brain regions in turtles. Thus, dorsal cortex in turtles appears to lack several of the major cell types characteristic of layers II-IV of mammalian isocortex, but possesses a number of the major cell types characteristic of layers V-VI of isocortex. The findings support and extend a previous suggestion by Ebner [1976], based on hodological data, that dorsal cortex in turtles may lack the types of neurons found in the more superficial layers of mammalian isocortex.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:A comparison of neurotransmitter-specific and neuropeptide-specific neuronal cell types present in the dorsal cortex in turtles with those present in the isocortex in mammals: implications for the evolution of isocortex. 168 5

The mechanisms underlying the age-related decrease and increase in somatotroph responsiveness to growth hormone-releasing factor (GHRF) and somatostatin respectively were studied in rat pituitary membranes in vitro. Basal adenylate cyclase (AC) activity was similar in pituitary membranes from rats of 8 days (either sex) and male rats of 3 months, but it was almost threefold higher in membranes from male rats of 21-23 months. GHRF induced a lower percentage stimulation of AC activity in membranes from infant and old than adult rats. Somatostatin inhibited stimulation of AC induced by forskolin more effectively in membranes from adult than infant and old rats. In parallel experiments, since the tissue we used is formed by a mixed population of pituitary cells, we evaluated, for comparison, the effect on AC of neurohormones, i.e. vasoactive intestinal polypeptide (VIP) and dopamine which act primarily on lactotrophs. VIP induced a lower fold-stimulation of AC activity in membranes from infant and old than adult rats. Dopamine inhibited forskolin-induced stimulation of AC in the following rank order of magnitude: old, adult and infant rats, and was also more effective in inhibiting basal AC activity in old than in adult rats. The stimulatory and inhibitory G proteins (Gs and Gi) coupled to AC were measured indirectly by evaluating stimulatory and inhibitory effects of different concentrations of GTP on AC. GTP, at stimulatory concentrations, increased AC activity in membranes from infant and adult rats similarly whereas its effect was significantly greater in membranes from old rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Age-related changes of growth hormone secretory mechanisms in the rat pituitary gland. 168 89

Histochemical changes in peptidergic and catecholaminergic neurons during ischemia were investigated in the cerebral neocortex of the gerbil. Catecholaminergic fibers were observed by catecholamine histofluorescence with glyoxylic acid solution, and peptidergic neuron systems such as vasoactive intestinal polypeptide (VIP), somatostatin (SOM), and neuropeptide Y (NPY) were observed by immunohistochemistry. Two hours after unilateral occlusion of the internal carotid artery, catecholaminergic fibers disappeared in the neocortex on the occlusion side, while peptidergic nerve fibers except for NPY fibers were intact after 2 hours of ischemia. NPY fibers had decreased in number on the occlusion side 2 hours after ischemia. VIP-, SOM-, and NPY-immunoreactive neurons showed a decrease of 60% six hours after ischemia, and these neurons completely disappeared in the cerebral neocortex 24 hours after ischemia. These results suggest that catecholaminergic neuron system is more vulnerable than the peptidergic one in ischemic event.
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PMID:[Selective vulnerability of peptide-containing neurons in cerebral ischemia; immunohistochemical study]. 168 33

Endocrine cells in the gastrointestinal tract of the domestic duck were identified immunocytochemically using antisera specific to bombesin, chromogranin A, cholecystokinin (CCK), gastrin, glucagon, neuron specific enolase (NSE), neurotensin, secretin, 5-hydroxytryptamine (5-HT), somatostatin, substance P and vasoactive intestinal polypeptide (VIP). Chromogranin A, 5-HT and somatostatin immunoreactive cells were widespread throughout the gastrointestinal tract. Bombesin immunoreactive cells were observed only in the proventriculus and the gizzard. CCK, substance P and neurotensin immunoreactive cells were present in the intestinal tracts from the duodenum to the colorectum. The latter were numerous also in the antrum. Gastrin cells were peculiar to the antrum but present also in the gizzard and small intestine. Glucagon immunoreactive cells were present in the jejunum-ileum and above all in the large intestine. Only few secretin cells were present in the duodenum. The highest frequency of endocrine cells was found in the antrum, while the lowest was observed in the caeca. Antisera to somatostatin and substance P showed numerous nerve cells and fibers besides endocrine cells, whereas NSE and VIP immunopositivity was found in the nervous structures only of the gut wall.
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PMID:An immunohistochemical study on the endocrine cells in the gastrointestinal tract of domestic duck. 168 96

The pituitary hormones prolactin and oxytocin play important roles in the production and ejection of milk. In addition, some gastrointestinal peptides are released in response to suckling. During suckling, the piglets massage the udder of the sow both before and after let-down and the duration of suckling is correlated to the amount of milk produced by the sow. The aim of this study was to investigate whether there is a quantitative relation between the release of prolactin, gastrin, somatostatin, insulin, glucagon and vasoactive intestinal polypeptide (VIP) and the amount of stimulation of the sow's teats by the piglets. Repeated blood samples were drawn from three Swedish Landrace sows during three consecutive nursings by each sow on days 1, 3, 7 and 14 after parturition. The duration of massage by the piglets was noted, as was the number of piglets massaging. Hormone levels were quantified by radioimmunoassay. The release of prolactin, somatostatin, insulin, glucagon and VIP but not of gastrin were found to be significantly related to the amount of teat massage performed by the piglets during the first 2 weeks of lactation. The release was related to the duration of piglet massage or to the combined effect of duration and the number of piglets massaging but not to the number of piglets massaging per se. The basal level of prolactin was found to decrease during this time.
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PMID:Quantitative relationships between suckling-induced teat stimulation and the release of prolactin, gastrin, somatostatin, insulin, glucagon and vasoactive intestinal polypeptide in sows. 168 75

The rat glucagon gene 5'-flanking region contains a pancreatic islet-specific enhancer-like element, G3. It has been shown previously that G3-binding and transactivating proteins are present in islet cell lines expressing the glucagon, somatostatin, and insulin genes, but not in several nonislet cell lines. The present study now shows that the glucagon G3 transcription factor binds to DNA sequences within cis-acting elements of the rat somatostatin and rat insulin-I genes that have been defined by others as pancreatic islet-specific transcriptional enhancers. In addition, when fused to glucagon or somatostatin minimal promoters in reporter plasmids, these enhancer elements of the three islet hormone-producing genes functionally activate transcription when transfected into islet cell lines producing glucagon, insulin, or somatostatin. The enhancer elements of the three different islet polypeptide hormone genes define a potential consensus motif that binds islet cell type-specific transcription factors.
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PMID:The pancreatic islet-specific glucagon G3 transcription factors recognize control elements in the rat somatostatin and insulin-I genes. 168 54


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