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 neuropeptides somatostatin, neurotensin and substance P were investigated in rats during and after limbic seizures induced by systemic injection of kainic acid (10 mg/kg, i.p.). Three hours after injection of the toxin, pronounced decreases (40-50%) in somatostatin-like immunoreactivity in frontal cortex, striatum, dorsal hippocampus and amygdala/pyriform cortex were observed. Concomitantly, neurotensin-like and substance P-like immunoreactivities were also reduced in the frontal cortex and the hippocampus. These early decreases in peptide levels may result from increased release and subsequent inactivation of the peptides during acute seizures. At later time intervals, 3, 10 and 30 days after injection of kainic acid, the initially decreased peptide levels were partially normalized. However, the reduction in somatostatin-like immunoreactivity in amygdala/pyriform cortex and striatum persisted up to 30 days. Neurotensin-like immunoreactivity remained decreased in the frontal cortex. On the other hand, neurotensin- and substance P-like immunoreactivities were increased in the striatum and substantia nigra 10-30 days after injection of kainic acid. These late changes in peptide levels may suggest destruction of peptidergic neurons or adaptive changes induced by the convulsions. Pretreatment of rats with cysteamine (100 mg/kg, i.p.), an agent which decreases brain somatostatin levels, had no effect on the intensity of kainic acid induced convulsions, although a slightly earlier onset of seizures was observed. The changes in peptide levels, especially the marked decreases in somatostatin content after systemic injection of kainic acid, suggest considerable acute and chronic alterations in peptidergic systems caused by limbic convulsions.
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PMID:Kainic acid induced seizures: changes in somatostatin, substance P and neurotensin. 242 20

The presence and distribution of multiple neuropeptides in vagal and glossopharyngeal afferent ganglia of the rat were studied using immunohistochemistry. Substance P-, calcitonin-gene related peptide-, cholecystokinin-, neurokinin A-, vasoactive intestinal polypeptide-, and somatostatin-immunoreactive neurons were detected in each visceral afferent ganglion. Neurotensin-immunoreactive cells were not observed. In the nodose ganglion (inferior ganglion of the vagus nerve) occasional immunoreactive cells were scattered throughout the main (caudal) portion of the ganglion with small clusters of cells seen in the rostral portion. The pattern of distribution of the various peptides in the nodose ganglion was similar, with the exception of vasoactive intestinal polypeptide-immunoreactive neurons which exhibited a more caudal distribution. The relative numbers of immunoreactive cells varied, with the greatest numbers being immunoreactive for substance P or vasoactive intestinal polypeptide, and the lowest numbers being immunoreactive for neurokinin A and somatostatin. A build-up of immunoreactivity for each of the peptides, except somatostatin and neurotensin, was detected in vagal nerve fibers of colchicine-injected ganglia. Numerous peptide-immunoreactive cells were also found in the petrosal (inferior ganglion of the glossopharyngeal nerve) and jugular (superior ganglion of the vagus nerve) ganglia. No specific intraganglionic distribution was noted although the relative numbers of cells which were immunoreactive for the different peptides varied considerably. Substance P and calcitonin-gene related peptide were found in large numbers of cells, cholecystokinin was seen in moderate numbers of cells, and neurokinin A, vasoactive intestinal polypeptide and somatostatin were seen in fewer cells. These data provide evidence for the presence and non-uniform distribution of multiple peptide neurotransmitters in vagal and glossopharyngeal afferent neurons. In general, relatively greater numbers of immunoreactive cells were located in the rostral compared with caudal nodose ganglion, and in the petrosal and jugular ganglia compared with the nodose ganglion. Thus, multiple neuropeptides may be involved as afferent neurotransmitters in the reflexes mediated by vagal and glossopharyngeal sensory nerves.
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PMID:Immunohistochemical study of neuropeptides in vagal and glossopharyngeal afferent neurons in the rat. 245 28

A culture system of dispersed submucosal neurons from canine ileum has been developed. The neuronal nature of over 80% of the cells in culture was confirmed by positive staining with a neurofilament antibody. In this culture system, neurotensin-immunoreactive neurons constituted greater than 50% of the total cell population. Neurotensin immunoreactivity in these cells was chromatographically characterized as a single molecular form coeluting with synthetic neurotensin (1-13). We have assessed the release of immunoreactive neurotensin by stimulatory and inhibitory transmitters, and by post-receptor activators of cell function. Forskolin (10 microM), the calcium ionophore A23187 (100 nM), and the active phorbol ester beta-12 myristrate 13-acetate (10 nM), each significantly increased neurotensin release compared with basal peptide secretion. The concomitant application of ionophore and phorbol ester resulted in a marked increase in neurotensin release and this stimulatory response was inhibited over 70% by somatostatin (100 nM). Substance P (0.1-100 nM) caused a dose-dependent increase in neurotensin release. Somatostatin (100 nM) reduced maximal stimulation with 100 nM substance P by 79%. Our results suggest that this submucosal culture system represents an entirely new model for characterizing transmitter release from enteric neurons.
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PMID:Canine enteric submucosal cultures: transmitter release from neurotensin-immunoreactive neurons. 251 2

The concentration of 5 neuropeptides, neurotensin (NT), somatostatin (SRIF), corticotropin-releasing factor (CRF), bombesin and thyrotropin-releasing hormone (TRH) was measured in 3 cerebrocortical areas and several subcortical regions in post-mortem brains obtained from patients with histologically verified Alzheimer's disease and from controls without neurological or psychiatric disorders using sensitive and specific radioimmunoassay procedures. In Alzheimer's disease, reductions in the concentration of SRIF and CRF were observed in frontal and temporal cortex. In addition, in Alzheimer's disease, SRIF was also reduced in concentration in the hypothalamus, whereas CRF concentrations were reduced in the caudate nucleus. Neurotensin was reduced in concentration in the amygdala in Alzheimer's disease. No alterations in TRH or bombesin/gastrin-releasing peptide were found. These findings provide further evidence for the pathological involvement of certain neuropeptide-containing neurons in Alzheimer's disease.
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PMID:Neuropeptides in Alzheimer's disease: a postmortem study. 256 90

Neurotensin, bradykinin and somatostatin inhibited in a time- and concentration-dependent manner prostaglandin E1- or forskolin-stimulated cAMP production in neuroblastoma N1E115 cells. Cell treatment with 1 microgram/ml pertussis toxin for 6 hours reversed the inhibition elicited by peptides after short incubation periods (less than or equal to 1 min) but, in contrast, had no effect after longer incubation periods (greater than or equal to 3 min). Fluoroaluminate also inhibited prostaglandin E1-stimulated cAMP production in N1E115 cells, and this effect was not reversed by pertussis toxin. The 6 hour treatment with pertussis toxin was shown to be sufficient to ADP ribosylate virtually all of the 41 kD protein substrate corresponding to the alpha subunit of Gi. Protein kinase C activation with phorbol ester did not inhibit basal or stimulated cAMP production. Our data point to the existence of both pertussis toxin sensitive and insensitive mechanisms of neuropeptide-mediated inhibition of cAMP formation in N1E115 cells. The toxin insensitive response is not mediated by protein kinase C. The possibility is discussed that it results from the activation of a pertussis toxin insensitive G protein.
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PMID:Neurotensin, bradykinin and somatostatin inhibit cAMP production in neuroblastoma N1E115 cells via both pertussis toxin sensitive and insensitive mechanisms. 256 13

Enteroendocrine cells immunoreactive for gastrin, bovine pancreatic polypeptide (BPP), glucagon (glicentin), 5-hydroxytryptamine (5-HT), somatostatin, secretin, motilin, gastric inhibitory peptide (GIP) and cholecystokinin (CCK) are scattered throughout the small intestinal epithelium of the newborn opossum and in all later postnatal stages examined. The number of BPP- and glucagon-immunoreactive cells is relatively high in the newborn and rapidly decreases until only occasional cells are present after the first postnatal week. Cells immunoreactive for GIP, CCK, 5-HT, motilin, gastrin and secretin increase in number with development. Secretin-, motilin-, CCK- and GIP-immunoreactive cells generally are concentrated proximally in the small intestine and as they increase in number, differentiate in more distal regions. The number of gastrin-immunoreactive cells actually decreases just prior to weaning but then increases at and after, weaning. Neurotensin-immunoreactive cells are unusual in that they do not appear until about the 74th postnatal day and then are first encountered in the distal small intestine. As development progresses they increase in number and appear in the more proximal regions. Cells immunoreactive for 5-HT at first increase but then decrease sharply at weaning only to increase markedly again after this time. In contrast, somatostatin-immunoreactive cells gradually decrease in number until weaning then dramatically increase. If the total number of enteroendocrine cells in the small intestine is considered, there is a gradual decrease from birth until weaning when a dramatic increase occurs. Cells immunoreactive for neurotensin, 5-HT and somatostatin are also found in the intestinal epithelium of the developing colon and caecum. Somatostatin- and 5-HT-immunoreactive cells are found throughout the colon in the newborn whereas neurotensin-immunoreactive cells, although observed initially in the proximal colon, do not form a significant population until weaning and then are concentrated distally.
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PMID:Enteroendocrine cells in the developing opossum small intestine and colon. 280 25

We have examined the effects of several neuropeptides on the release of immunoreactive somatostatin from cerebral cortical cells in vitro. Neurotensin and vasoactive intestinal polypeptide induced large increases in somatostatin release, whereas cholecystokinin, gonadotropin releasing hormone and Met-enkephalin induced only modest increases. Thyrotropin releasing hormone and insulin had no effect. These results demonstrate a complex interaction amongst neuropeptides in the cerebral cortex, which must be considered in future studies of the roles of peptides in cortical function.
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PMID:The effects of neurotensin, vasoactive intestinal polypeptide and other neuropeptides on the secretion of somatostatin from cerebral cortical cells. 285 7

The ability of certain neuropeptides (glucagon, somatostatin, leu-enkephalin and neurotensin) to release known neurotransmitters (glycine, GABA, dopamine and 5-hydroxytryptamine) was tested in the chicken retina. Tritiated neurotransmitters were injected intravitreally in chicken eyes. After excision, the retina was stimulated in vitro with the neuropeptide in micromolar concentrations while monitoring the efflux of radioactivity from the retina. A rise of the efflux represents a stimulus dependent release. Neurotensin release [3H] glycine, [3H]dopamine and [3H]5-hydroxytryptamine. Leu-enkephalin released [3H]dopamine and somatostatin released [3H]5-hydroxytryptamine. Glucagon was without effect. [3H]GABA was not released by any of the neuropeptides.
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PMID:Neurotransmitter release by certain neuropeptides in the chicken retina. 286 56

The peptide content of the intercalated nuclei (ICN) of the amygdala and their projection to the parabrachial nucleus was studied in the rat using the combined retrograde transport-immunofluorescence method. Neurotensin, and to a lesser extent, corticotropin-releasing factor and somatostatin, were found within ICN neurons which innervate the parabrachial nucleus. Enkephalin and somatostatin terminals were particularly dense around ICN neurons that project to the parabrachial nucleus. Our results indicate a functional link between the ICN and the lateral subdivision of the central nucleus of the amygdala based on their similar peptidergic projections to the parabrachial nucleus.
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PMID:Peptidergic efferents from the intercalated nuclei of the amygdala to the parabrachial nucleus in the rat. 286 98

The jejunal contraction patterns of dogs in response to intravenous infusion of neurotensin, somatostatin, secretin, and met-enkephalin were analyzed. The peptides were given after administration of a noncaloric viscous cellulose meal. A computer was used to determine the length of spread of contraction waves, their contraction force, the contraction frequency, and the motility index. Transit rates of luminal content were assessed videofluoroscopically. During saline infusion the cellulose meal was propelled aborally at a transit rate of 3.1 +/- 1.1 cm/s; the corresponding length of spread of contraction waves was 10.3 +/- 1.5 cm. All peptides decreased both the transit rate (0.45-1.81 cm/s) and the contraction spread (3.7-6.2 cm). Neurotensin increased the contraction force, but had no effect on contraction frequency and motility index. The other peptides reduced the motility index and the frequency and force of contractions. It was shown that the peptides influenced intestinal contraction patterns and the transit rate of luminal content. The length of spread of contraction waves was found to be most important in the regulation of transit.
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PMID:Effects of neurohormonal agents on jejunal contraction spread and transit in the fed dog. 287 Sep 53


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