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)

The neuroendocrine regulation of pulsatile growth hormone (GH) secretion involves the reciprocal interactions between growth hormone-releasing hormone (GHRH)- and somatostatin-containing neurones, residing primarily in the hypothalamic arcuate nucleus (ARC) and the periventricular nucleus (PeN), respectively. Considerable evidence supports the concept that GH itself participates in the regulation of its own rhythmic secretion through a reciprocal feedback on GHRH and somatostatin neurones. The direct actions of GH are mediated through GH receptors, and in the PeN, the majority of somatostatin neurones express this receptor. GH induces the expression of the immediate early gene c-fos in the ARC; however, few GHRH residing in the ARC express the GH receptor, suggesting that the action of GH on GHRH cells must be indirect through another population of unidentified cells. NPY neurones express c-fos in response to GH, and preliminary results suggest that NPY neurones in the ARC express the GH receptor. These observations suggest that NPY neurones play a physiological role in the feedback of regulation of GH secretion.
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PMID:Role of NPY neurones in GH-dependent feedback signalling to the brain. 880 21

Colonic mucosal cells are known to contain several neuropeptides. The distribution of various peptide-containing cells in the colon and their possible modulation by aging and diet are unknown. We quantitated various peptide-containing cells from male Lobund-Wistar rat colon at 2, 22, 28, 30 and 33 months of age using indirect immunohistochemical techniques for several peptides including: neuropeptide Y, peptide YY, somatostatin, and chromogranin A. Four diets, varying in total calories and fat content, were examined. Serum gastrin was quantified by RIA at 2 and 33 months. Only NPY-, PYY- and SOM-positive cells were found in the colon. The number per crypt of neuropeptide Y-positive (0.55 +/- 0.04 at 2 months vs 0.80 +/- 0.22 at 33 months, P = 0.015) and peptide YY-positive cells increased with age. Staining for somatostatin and chromogranin, a marker for all enterochromaffin (EC) cells, revealed no change with aging. Diet did not influence the numbers of any peptide-containing cell. Serum gastrin was not different between the groups. A specific increase in NPY- and PYY-positive cells occurs in the aged rat colon. The extent to which this change may be related to age-related colonic dysmotility seen in elderly humans is worthy of exploration.
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PMID:Neuropeptide Y- and peptide YY-containing colonic cells increase with ageing in male rats. 891 66

We have previously shown that dark rearing moderates the normal decline in the number of somatostatin (SRIF) and neuropeptide (NPY) neurons in the developing rat visual cortex. Thus, cortical areas of visually deprived animals at postnatal day (P) 60 contain consistently more SRIF and NPY neurons than do the same areas of rats reared in normal lighting conditions. In present study animals were reared in darkness from birth to P14, P21, P30 or P60 and then placed in ambient light conditions up to the day of sacrifice (P60 or P90). Counting of immunocytochemically identified SRIF and NPY neurons in all cortical visual areas of these and of undeprived animals, showed that interruption of visual deprivation during both the early or the late stages of postnatal development restores the normal density of the above peptidergic neurons.
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PMID:Interruption of visual deprivation during development restores the normal density of peptidergic neurons in the rat visual cortex. 896 70

In the present study, we have investigated the effect in vitro of gastrin-releasing peptide (GRP, 10(-10) M), neuropeptide Y (NPY, 10(-10) M), somatostatin (10(-10) M) and vasoactive intestinal peptide (VIP, 10(-9) M) on the production of IL-1 beta, IL-6 and TNF alpha by peripheral whole blood cells from healthy young and old people. We have found that GRP, NPY, somatostatin and VIP stimulated the production of IL-1 beta in old subjects, and NPY, somatostatin and VIP in young ones. In addition, the production of IL-6 was enhanced by GRP, NPY and VIP in young and old people. The TNF alpha production was stimulated by NPY and somatostatin in young subjects, and by NPY, somatostatin and VIP in old ones, whereas GRP produced a decrease of TNF alpha in young persons. GRP in old subjects and VIP in young and old subjects stimulated in a great degree the LPS-induced IL-6 production by whole blood cells. On the contrary, GRP and VIP inhibited highly the LPS-induced TNF alpha production in young controls. Our results show that these neuropeptides, when added to whole blood cells at physiological concentrations, are able to stimulate the production of IL-1 beta, IL-6 and TNF alpha in a differential way according to the subject age.
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PMID:Differential effects of gastrin-releasing peptide, neuropeptide Y, somatostatin and vasoactive intestinal peptide on interleukin-1 beta, interleukin-6 and tumor necrosis factor-alpha production by whole blood cells from healthy young and old subjects. 898 99

Primary cultures of postganglionic sympathetic neurons were established more than 30 years ago. More recently, these cultures have been used to characterize various neurotransmitter receptors that govern sympathetic transmitter release. These receptors may be categorized into at least three groups: (1) receptors which evoke transmitter release: (2) receptors which facilitate; (3) receptors which inhibit, depolarization-evoked release. Group (1) comprises nicotinic and muscarinic acetylcholine receptors, P2X purinoceptors and pyrimidinoceptors. Group (2) currently harbours beta-adrenoceptors, P2 purinoceptors, receptors for PACAP and VIP, as well as prostanoid EP1 receptors. In group (3), muscarinic cholinoceptors, alpha 2- and beta-adrenoceptors, P2 purinoceptors, and receptors for the neuropeptides NPY, somatostatin (SRIF1) and LHRH, as well as opioid (delta and kappa) receptors can be found. Receptors which regulate transmitter release from neurons in cell culture may be located either at the somatodendritic region or at the sites of exocytosis, i.e. the presynaptic specializations of axons. Most of the receptors that evoke release are located at the soma. There ionotropic receptors cause depolarizations to generate action potentials which then trigger Ca(2+)-dependent exocytosis at axon terminals. The signalling mechanisms of metabotropic receptors which evoke release still remain to be identified. Receptors which facilitate depolarization-evoked release appear to be located preferentially at presynaptic sites and presumably act via an increase in cyclic AMP. Receptors which inhibit stimulation evoked release are also presynaptic origin and most commonly rely on a G protein-mediated blockade of voltage-gated Ca2+ channels. Results obtained with primary cell cultures of postganglionic sympathetic neurons have now supplemented previous data about neurotransmitter receptors involved in the regulation of ganglionic as well as sympatho-effector transmission. In the future, this technique may prove useful to identify yet unrecognized receptors which control the output of the sympathetic nervous system and to elucidate underlying signalling mechanisms.
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PMID:Receptors controlling transmitter release from sympathetic neurons in vitro. 908 89

Patients with Huntington's disease (HD) develop pathological changes in cerebral cortex as well as in striatum. We studied levels of neuropeptide immunoreactivity in 13 areas of postmortem cerebral cortex dissected from 24 cases of HD and 12 controls. Concentrations of immunoreactive cholecystokinin (CCK-LI) were consistently elevated 57 to 153% in HD cortex. Levels of vasoactive intestinal polypeptide (VIP-LI) and neuropeptide Y (NPY-LI) were significantly increased in 10 and 8 of the 13 cortical regions, respectively. Concentrations of somatostatin (SRIF-LI) were increased in only 3 areas, while substance P (SP-LI) was, for the most part, unchanged. Detailed analyses of the CCK-LI and VIP-LI data showed there to be no relationship between the increased cortical peptide levels and the degree of striatal atrophy. We studied the same cortical peptides in rats with long-standing striatal lesions and found no significant changes of CCK-LI, NPY-LI, VIP-LI, or SRIF-LI in any of the 8 cortical regions that were examined. These results indicate that there are widespread and differential changes in cortical neuropeptide systems in HD and that these changes occur independently of the striatal pathology that characterizes the illness.
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PMID:Cortical peptide changes in Huntington's disease may be independent of striatal degeneration. 912 12

The distribution and identity of the various endocrine cell types were examined in the pancreas, stomach, and anterior intestine of the phylogenetically ancient actinopterygian, the gar (Lepisosteus osseus L.), using immunohistochemistry. Antisera used were directed against several insulins (INSs) and somatostatins (SSTs), and members of the pancreatic polypeptide (PP, aPY, NPY) and glucagon (GLUC, GLP) families. In the gar pancreas the most pronounced aggregation of islet tissue is among the exocrine acini near the union of extrahepatic common bile duct with the gastrointestinal junction. Four immunoreactive cell types were identified within well-defined islets (A, B, D, and F cells) but immunoreactive cell types were also seen isolated among the exocrine acini. Centrally located B cells were immunoreactive with mammalian and lamprey INS antisera whereas the widely dispersed D cells immunostained with anti-SST-14, -25, and -34. SST was also localized in the epithelium of the pancreatic ducts. There was a colocalization of immunoreactivity for each member of the PP and GLU families at the periphery of each islet to identify F and A cells, respectively. However, colocalization of peptides from both families is suspected for at least some cells. Although the gastric and intestinal mucosae showed a similar pattern of immunoreactivity to GLP and not GLU, they had contrasting immunoreactivity with the two INS antisera. SST immunoreactivity was restricted to the stomach, whereas three of the four PP-family peptides were only immunoreactive in the intestine. Immunoreactivity to the various antisera used in the study imply that there may be an organ-specific processing of preproinsulin, that the gar SST profile may be more similar to agnathan and bowfin rather than either elasmobranch or teleost SSTs, and that only the GLP portion of the preproglucagon gene is expressed in the gastrointestinal mucosa. Our results are consistent with other recent endocrine studies showing that the gar is a widely distinct actinopterygian.
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PMID:An immunohistochemical study of the endocrine cells within the pancreas, intestine, and stomach of the gar (Lepisosteus osseus L.) 912 60

Histological, immunocytochemical and immunofluorescence methods were employed to study the intestine and endocrine pancreas of the elephant. The histological findings were in line with those in monogastric mammals. In the mucosa of intestine, endocrine cells were immunoreactive to somatostatin, gastrin, CCK, GIP, secretin, motilin, glucagon and NPY. Nerve cells immunoreactive to somatostatin, substance P, VIP, PHI, NPY, bombesin and CGRP were detected. No immunoreactivity to neurotensin was observed, islets of the pancreas had insulin cells in their cores and glucagon and somatostatin cells in their mantles. The antisera employed failed to demonstrate PP cells in the pancreas, but NPY-immunoreactive cells were present.
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PMID:The intestine and endocrine pancreas of the African elephant: a histological immunocytochemical and immunofluorescence study. 917 65

G-protein-coupled or 7-transmembrane receptors (7TMRs) are often studied after heterologous expression in mammalian cells such as COS-7, CHO-K1, or HEK-293s. In this paper, we describe the development of a rapid and generic method for producing stable Chinese hamster ovary cell lines expressing high levels of recombinant 7TMRs by N-terminal tagging these proteins with the hemagglutinin (HA) sequence. To illustrate the broad applicability of this technique, we have presented data from cell lines expressing a glycoprotein hormone receptor for follicle-stimulating hormone (FSHR), CXC- (CXCR-2), and CC-chemokine (CCR-1) receptors and peptide receptors from the somatostatin (SSTR1, 2, 5) and neuropeptide Y (NPY-Y2, -Y4 Rs) families. Typically, cell lines with a receptor density of 1 to 15 pmol/mg protein are produced with this method. The presence of the HA tag does not adversely affect the binding or functional activity of the receptors.
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PMID:A generic method for the production of cell lines expressing high levels of 7-transmembrane receptors. 923 98

To evaluate the relative ability of those striatal neuron types containing calbindin or parvalbumin to withstand a Ca(2+)-mediated excitotoxic insult, we injected the NMDA receptor-specific excitotoxin quinolinic acid (QA) into the striatum in mature adult rats and 2 months later examined the relative survival of striatal interneurons rich in parvalbumin and striatal projection neurons rich in calbindin. To provide standardization to the survival of striatal neuron types thought to be poor in Ca2+ buffering proteins, the survival was compared to that of somatostatin-neuropeptide Y (SS/NPY)-containing interneurons and enkephalinergic projection neurons, which are devoid of or relatively poorer in such proteins. The various neuron types were identified by immunohistochemical labeling for these type-specific markers and their relative survival was compared at each of a series of increasing distances from the injection center. In brief, we found that parvalbuminergic, calbindinergic, and enkephalinergic neurons all showed a generally comparable gradient of neuronal loss, except just outside the lesion center, where calbindin-rich neurons showed significantly enhanced survival. In contrast, striatal SS/NPY interneurons were more vulnerable to QA than any of these three other types. These observed patterns of survival following intrastriatal QA injection suggest that calbindin and parvalbumin content does not by itself determine the vulnerability of striatal neurons to QA-mediated excitotoxicity in mature adult rats. For example, parvalbuminergic striatal interneurons were not impervious to QA, while cholinergic striatal interneurons are highly resistant and SS/NPY+ striatal interneurons are highly vulnerable. Both cholinergic and SS/NPY+ interneurons are devoid of any known calcium buffering protein. Similarly, calbindin does not prevent striatal projection neuron vulnerability to QA excitotoxicity. Nonetheless, our data do suggest that calbindin may offer striatal neurons some protection against moderate excitotoxic insults, and this may explain the reportedly slightly greater vulnerability of striatal neurons that are poor in calbindin to ischemia and Huntington's disease.
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PMID:Relative resistance of striatal neurons containing calbindin or parvalbumin to quinolinic acid-mediated excitotoxicity compared to other striatal neuron types. 950 Sep 58


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