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)

Neuronal degeneration that occurs in both ischemia and degenerative neurologic illnesses may involve excitotoxic mechanisms. In the present study, we examined whether cortical lesions with agonists acting at subtypes of glutamate receptors result in selective patterns of neuronal death. Injections of quinolinic acid, NMDA, homocysteic acid, kainic acid (KA), and alpha-amino-3-hydroxy-5-methylisoxazole-4-proprionic acid (AMPA) were made at 2 sites in the dorsolateral frontoparietal cortex in rats. After 1 week, the cerebral cortex was either dissected for neurochemical studies, or animals were perfused for histologic evaluation. Concentrations of somatostatin (SS), neuropeptide Y (NPY), substance P (SP), cholecystokinin (CCK), and vasoactive intestinal polypeptide (VIP) were measured by radioimmunoassay, while amino acids and catecholamines were measured by high-performance liquid chromatography (HPLC) with electrochemical detection. NMDA agonists (quinolinic acid, homocysteic acid, and NMDA itself) resulted in dose-dependent reductions in glutamate and GABA, while SS, NPY, SP, CCK, and VIP were either unchanged or significantly increased in concentration. KA and AMPA at doses that resulted in comparable GABA depletions caused significant reductions in SS concentrations. Markers of cortical afferents were spared. All excitotoxins resulted in dose-dependent marked increases in uric acid concentrations. Histologic examination verified that lesions with NMDA agonists produced relative sparing of NADPH-diaphorase, SS, VIP, and CCK neurons. These results show that NMDA excitotoxin lesions result in a pattern of selective neuronal damage in the cerebral cortex that is similar to that which occurs in both ischemia and Huntington's disease.
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PMID:Neurochemical characterization of excitotoxin lesions in the cerebral cortex. 167 Jul 82

A 31-year-old patient with a clinical picture of obstructive jaundice had surgical treatment, and a primary carcinoid of the ampulla of Vater (VA) was found. The tumor was studied with light microscopy, immunohistochemistry, and electron microscopy. The neoplasm had histopathologic and cytopathologic features similar to those encountered in typical neuroendocrine neoplasms. It is interesting that immunohistochemical techniques disclosed the presence of vasointestinal polypeptide, cholecystokinin, and bombesin; however, unlike most neuroendocrine neoplasms arising in VA, no somatostatin-immunoreactive cells were found.
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PMID:Neuroendocrine carcinoma of the ampulla of vater. A case of absence of somatostatin in a vasoactive intestinal polypeptide-, bombesin-, and cholecystokinin-producing tumor. 167 Sep 74

An important component of neuronal development is the matching of neurotransmitter expression with the appropriate target cell. We have examined how peptide transmitter expression is controlled in a simple model system, the avian ciliary ganglion (CG). This parasympathetic ganglion contains 2 distinct types of neurons: choroid neurons, which project to vasculature in the eye's choroid layer and use somatostatin as a co-transmitter with ACh, and ciliary neurons, which innervate the ciliary body and iris and use ACh but no known peptide co-transmitter. We have found that the earliest developmental stage in which neurons with somatostatinlike immunoreactivity (SOM-IR) are consistently found in vivo is stage 30 (embryonic day 6.5), a time shortly after the extension of neurites to targets in the eye's choroid layer. In cell culture, CG neurons expressed SOM-IR in co-culture with choroid cells, but not when cultured with striated muscle myotubes or with ganglion non-neuronal cells. No significant differences in neuronal survival or in ChAT activity were observed under these different co-culture conditions, which suggests that somatostatin expression is independently regulated. The stimulation of somatostatin expression was also specific in that other neuropeptides commonly found in autonomic neurons [neuropeptide Y (NPY), substance P (SP), vasoactive intestinal polypeptide (VIP)] were not induced in the presence of choroid cells. The ability to stimulate SOM-IR was not contact dependent because a macromolecule of greater than or equal to 10 kDa in choroid-conditioned medium (ChCM) was found to stimulate somatostatin expression in a dosage-dependent fashion. The somatostatin-stimulating activity induced SOM-IR in more than 90% of CG neurons, as well as in retrogradely labeled ciliary neurons, which would not normally express SOM-IR. Thus, the expression of somatostatin in cultured CG neurons is regulated by a macromolecule produced by cells in the choroid layer, a target normally innervated in vivo by CG neurons expressing somatostatin.
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PMID:Stimulation of somatostatin expression in developing ciliary ganglion neurons by cells of the choroid layer. 167 9

The effect of an intravenous infusion of secretin (2.0 CU/kg/h) on serum prolactin (PRL) and estradiol levels and plasma levels of vasoactive intestinal polypeptide and somatostatin (SRIH) was studied in 8 healthy and normally cycling women during the midfollicular phase (cycle day 7), at midcycle (day 14), and during the midluteal phase (day 21) of the menstrual cycle. When compared to basal preinfusion levels, a significant decrease in serum PRL levels was observed at steady state concentrations of plasma secretion (+30 to +60 min) both during the follicular (p less than 0.03) and the luteal (p less than 0.0001) phases. At midcycle a nonsignificant decrease was observed. A significant and negative correlation existed between serum PRL and plasma secretin levels in the follicular phase (r = -0.33; p less than 0.05) and in the luteal phase (r = 0.73; p less than 0.0001). The plasma concentrations of SRIH increased significantly at steady state conditions of secretin at midcycle (p less than 0.02) and in the luteal phase (p less than 0.04), while no effect was found during the follicular phase. A significant and positive correlation between plasma levels of SRIH and secretin was observed at midcycle (r = 0.63; p less than 0.002) and in the luteal phase (r = 0.46; p less than 0.02). No effect of secretin on plasma vasoactive intestinal polypeptide and serum estradiol concentrations was demonstrated. These results suggest that the suppression of PRL in the follicular phase of the spontaneous menstrual cycle can be ascribed to an effect of secretin alone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prolactin response to secretin during the spontaneous menstrual cycle in women. 167 62

The mechanism of action of vasoactive intestinal polypeptide on gastric acid secretion was examined in the isolated, luminally perfused mouse stomach. Vasoactive intestinal polypeptide caused a weak, transient increase in basal and histamine-stimulated acid secretion and a sustained increase in somatostatin secretion. The sustained increase in somatostatin despite return of acid to basal levels indicated that somatostatin secretion was a direct response to vasoactive intestinal polypeptide and not mediated by intraluminal acidification. The increase in somatostatin secretion was partly responsible for the weak, transient nature of the acid response since incubation with pertussis toxin, which is known to block the inhibitory effect of exogenous and endogenous somatostatin, converted the acid response to a sustained increase throughout the period of stimulation. The inhibitory influence of somatostatin was confirmed with selective vasoactive intestinal polypeptide antagonists. The antagonists inhibited vasoactive intestinal polypeptide-induced somatostatin secretion but caused a sustained increase in acid secretion. The pattern of response implied that somatostatin secretion was more sensitive than acid secretion to vasoactive intestinal polypeptide and vasoactive intestinal polypeptide antagonists and that suppression of somatostatin eliminated the main inhibitory influence on acid secretion. In addition, both vasoactive intestinal polypeptide antagonists inhibited basal somatostatin secretion, implying that input from tonically active vasoactive intestinal polypeptide neurons is responsible, at least in part, for basal somatostatin secretion.
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PMID:The effect of vasoactive intestinal polypeptide on gastric acid secretion is predominantly mediated by somatostatin. 167 56

Upon investigation of pig intestinal peptides for effects on the release of endocrine hormones from the isolated perfused rat pancreas, we reported earlier that glucose-stimulated insulin release was inhibited by PEC-60, a peptide with marked sequence similarity to PSTI (pancreatic secretory trypsin inhibitor). Continuing this study we found a polypeptide, which inhibited glucose-induced insulin release but enhanced glucose-induced somatostatin secretion. Determination of the amino acid sequence of this polypeptide revealed that it is identical to that of PSTI. Thus, PSTI modulates islet hormone release.
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PMID:Pancreatic secretory trypsin inhibitor (PSTI) isolated from pig intestine. Influence on insulin and somatostatin release. 167 2

Although neuropeptides have been demonstrated to be hippocampal neuromodulators in laboratory animals, their role in human hippocampal physiology or pathophysiology remains to be defined. The concentrations of somatostatin, cholecystokinin octapeptide, vasoactive intestinal polypeptide, and dynorphin A 1-17 were determined in hippocampal tissue resected from patients with cryptogenic temporal lobe epilepsy, a common seizure disorder originating in or near the hippocampus. Control tissue was obtained from cadavera or epilepsy patients in whom the hippocampus was removed during the resection of temporal lobe tumors. Peptide determinations were performed on extracts of punch biopsy specimens taken from six different hippocampal regions. A significant decrease in immunoreactive somatostatin concentration was identified in the dentate gyrus and in region cornu ammonis 4 of cryptogenic temporal lobe epilepsy specimens. No significant changes were present in any other hippocampal region or in the levels of other peptides. In situ hybridization studies performed on cryostat sections from similar patients confirmed a marked loss of neurons expressing the somatostatin gene, which was restricted to the dentate hilus. The density of specific 125I-somatostatin binding to cryostat sections, as determined by semiquantitative in vitro autoradiography, was significantly increased in the dentate gyrus of the cryptogenic epilepsy patients, compared with tumor control specimens. We conclude that a loss of somatostatin-producing interneurons with an upregulation of dentate somatostatin receptors is a specific and characteristic element in the pathophysiology of human cryptogenic temporal lobe epilepsy.
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PMID:A selective loss of somatostatin in the hippocampus of patients with temporal lobe epilepsy. 167 46

Effects of the mesenteric nerve stimulation (MNS) on the twitch contraction induced by field stimulation were investigated regarding the relationship between myenteric neurons and extrinsic cholinergic nerves in the guinea-pig mesenteric nerve-ileal preparation. The twitch contraction was inhibited after MNS. The inhibition of the twitch contraction after MNS was induced twice, just after MNS (1st inhibition) and 2-3 min later (2nd inhibition) (type I), or once, just after MNS (1st inhibition) (type II), in recovery course of twitch contraction for 6-8 min. The 1st inhibition was slightly decreased by guanethidine and hexamethonium. The inhibitory response (1st inhibition) in both types I and II was recovered to the control level by pretreatment with naloxone (recovered twitch contraction), but the late inhibitory response (2nd inhibition) was markedly observed after 2-3 min in types I and II. Either the 1st or the 2nd inhibition was not altered by capsaicin, desensitization to calcitonin gene-related polypeptide (CGRP), vasoactive intestinal polypeptide (VIP), somatostatin, or galanin. The recovered twitch contraction in types I and II was decreased by CGRP-desensitization, or capsaicin. These results suggest that the first inhibitory response was induced by enteric opioid neurons connected with extrinsic cholinergic nerves, but the 2nd inhibition was induced by unknown substances other than CGRP, VIP, somatostatin, and galanin. The twitch contraction may partly be induced by endogenous neurokinin-like substances. And, some CGRP containing neurons, which connect with extrinsic cholinergic nerves, probably activate the intrinsic excitatory neurons.
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PMID:Interaction of myenteric neurons and extrinsic nerves in the intestinal inhibitory response induced by mesenteric nerve stimulation. 167 43

Duodenal biopsies obtained from seven normal subjects and six ulcerous patients were cultured in vitro for 30 min at 37 degrees C under various experimental conditions. Epidermal growth factor (EGF) and somatostatin released in the culture medium were determined by radioimmunoassay. Under basal conditions, EGF and somatostatin levels were significantly higher in normal subjects (11.49 +/- 3.07 ng/mg protein and 3.06 +/- 0.8 ng/mg protein, respectively) than in ulcerous patients (6.9 +/- 1.98 ng/mg protein and 1.75 +/- 1.23 ng/mg protein, respectively). However, when antibodies to somatostatin and vasoactive intestinal polypeptide (VIP) were added together to the culture media, in ulcerous patients, EGF levels also were lower as absolute values, but were higher as a percentage of variation than controls (p less than 0.05). The fall of EGF secretion from tissue cultures of ulcerous patients could be the consequence of endocrine cellular loss or damage, rather than the cause of ulceration. Moreover, the EGF-producing cells around the lesion in ulcerous patients seems to be hyperactive, and this hyperfunction of EGF-producing cells might contribute to the in vivo repair of tissue damage.
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PMID:The role of epidermal growth factor in the pathogenesis of peptic ulcer disease. 167 87

Somatostatin gene fragment extracted and purified from plasmid pSom5 bacterium was ligated with the plasmid pBD2 DNA. Transformation of E. coli D29A1 with the chimeric plasmid DNA led to the synthesis of a polypeptide including the sequence of amino acids corresponding to somatostatin. The chimeric protein (50000 dalton) was purified and characterized by the beta-galactosidase affinity chromatography and the expression of the somatostatin gene in E. coli D29A1 is certain after the radioimmunoassay of the chimeric protein and its mixture by treatment with cyanogen bromide.
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PMID:[Expression of somatostatin gene in E. coli D29A1]. 167 42


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