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)

GABAergic and cholinergic synaptosomes from rat cerebral cortex were isolated by a magnetic immunoaffinity technique, i.e. immunomagnetophoresis. These subpopulations were extracted and subjected to radioimmunoassay for four neuropeptides: Neuropeptide Y (NPY); vasoactive intestinal peptide (VIP); substance P (SP); and somatostatin (SRIF). In each of the sub-populations three of the four peptides were enriched in the sorted fraction compared with the mother fraction with respect to the cytosolic marker lactate dehydrogenase (LDH). In the GABAergic sub-population the order was SP > SRIF > NPY > or = VIP whilst in the cholinergic sub-population they were enriched in the order VIP > or = NPY > SP > SRIF. The presence of NPY has not previously been reported in cortical cholinergic neurons.
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PMID:The presence of neuropeptides in GABAergic and cholinergic rat cerebrocortical synaptosome sub-populations. 145 55

Cholinergic synaptosomes from rat cerebral cortex were isolated by a magnetic immunoaffinity technique, i.e. immunomagnetophoresis. This subpopulation was extracted and subjected to radioimmunoassay for 4 neuropeptides:neuropeptide Y (NPY); vasoactive intestinal peptide (VIP); substance P (SP); and somatostatin (SRIF). Three of the 4 neuropeptides were enriched in the sorted fraction compared with the mother fraction with respect to the cytosolic marker lactate dehydrogenase (LDH). The most enriched neuropeptide was NPY followed by SP and VIP. Somatostatin was not enriched in the cholinergic synaptosome subpopulation. The presence of NPY has not previously been reported in cortical cholinergic neurones.
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PMID:Neuropeptide content of purified rat brain cholinergic synaptosome subpopulations. 160 51

Functional vasoactive intestinal peptide (VIP) receptors have been characterized in rat peritoneal macrophages. The binding depended on time, temperature and pH, and was reversible, saturable and specific. Scatchard analysis of binding data suggested the presence of two classes of binding sites: a class with high affinity (kd = 1.1 +/- 0.1 nM) and low capacity (11.1 +/- 1.5 fmol/10(6) cells), and a class with low affinity (kd = 71.6 +/- 10.2 nM) and high capacity (419.0 +/- 80.0 fmol/10(6) cells). Structural requirements of these receptors were studied with peptides structurally or not structurally related to VIP. Several peptides inhibited 125I-VIP binding to rat peritoneal macrophages with the following order of potency: VIP greater than rGRF greater than hGRF greater than PHI greater than secretin. Glucagon, insulin, somatostatin, pancreastatin and octapeptide of cholecystokinin (CCK 26-33) were ineffective. VIP induced an increase of cyclic AMP production. Half-maximal stimulation (ED50) was observed at 1.2 +/- 0.5 nM VIP, and maximal stimulation (3-fold above basal levels) was obtained between 0.1-1 microM. Properties of these binding sites strongly support the concept that VIP could behave as regulatory peptide on the macrophage function.
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PMID:Characterization of functional receptors for vasoactive intestinal peptide (VIP) in rat peritoneal macrophages. 165 77

In recent years evidence has accumulated indicating the presence of functional receptors for most neurotransmitters on astrocytes. In particular, receptors coupled to adenylate cyclase have been demonstrated, in primary astrocyte cultures, for vasoactive intestinal peptide (VIP), noradrenaline (NA) and adenosine. Here we provide, in primary cultures of cerebral cortical astrocytes prepared from neonatal mice, a detailed characterization of a cAMP-dependent process elicited by VIP, NA and adenosine, i.e. the hydrolysis of glycogen. The EC50s for the glycogenolytic effect of VIP, NA and adenosine are 3, 20 and 800 nM, respectively. The initial rate of glycogen hydrolysis is, in nmol/mg prot/min, 9.1 for VIP and 7.5 for NA. The effect of NA is predominantly mediated by beta-adrenoceptors, although an alpha 1-adrenergic component, acting most likely through protein kinase C activation, is also present. The action of VIP is mimicked by peptides sharing sequence homologies such as PHI and secretin. Glutamate, GABA, carbachol and the peptides NPY and somatostatin do not influence glycogen levels. The glycogen content of the cultures can be markedly increased by anabolic factors present in fetal calf serum, by high (e.g. 25 mM) glucose in the medium and by 48-h pretreatment of the cultures with dibutyryl cAMP. These results indicate that the glycogen content of astrocytes is under the dynamic control of various factors, including certain neurotransmitters. They also further stress the notion of a functional interaction between neurons and glial cells aimed at maintaining local energy metabolism homeostasis.
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PMID:Characterization of the glycogenolysis elicited by vasoactive intestinal peptide, noradrenaline and adenosine in primary cultures of mouse cerebral cortical astrocytes. 166 73

The isolated gastric gland preparation, with aminopyrine accumulation as an index of the parietal cell response, has been used to study the effects of somatostatin (S-14), gastrin-releasing peptide (GRP), cholecystokinin (CCK-8), vasoactive intestinal peptide (VIP), and peptide YY (PYY) on the in vitro acid secretion in human and rabbit oxyntic mucosa. Somatostatin was able to inhibit the parietal cell response to histamine in both human and rabbit isolated gastric glands (maximal inhibition, 22% and 34%, respectively) but failed to inhibit the parietal cell response to db-cAMP. However, other peptides capable of inhibiting gastric acid secretion in vivo, such as CCK, VIP, and PYY, were unable to induce any inhibition of the parietal cell response to db-cAMP or histamine in the isolated gastric gland preparation irrespective of the species studied. GRP was not able to induce a parietal cell response, a finding that is in accord with the assumption that the stimulatory effect of GRP on gastric acid secretion in vivo is by releasing gastrin from antral G-cells.
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PMID:Effects of some gastrointestinal peptides on isolated human and rabbit gastric glands. 167 70

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

Delta-sleep-inducing peptide (DSIP), vasoactive intestinal peptide (VIP), peptide YY (PYY) and somatostatin (SOM) were assayed with specific radioimmunological methods in cerebrospinal fluid (CSF) of healthy volunteers, 12 patients with Alzheimer's disease (AD), 11 patients with multi-infarct dementia (MID) and 10 patients with normal-pressure hydrocephalus (NPH). Patients with NPH were reinvestigated 3 months after a ventriculoperitoneal shunt operation. DSIP, PYY and SOM levels in CSF were decreased in patients with NPH compared to controls. The CSF concentration of SOM was also significantly reduced in patients with AD. No correlations were found between the degree of dementia in any of the illnesses and the CSF concentrations of the peptides. The concentration of DSIP, VIP and SOM increased significantly in parallel to the clinical improvement after the shunt operation in NPH patients.
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PMID:Neuropeptides in cerebrospinal fluid in normal-pressure hydrocephalus and dementia. 167 71

In light of the effects of gastrointestinal (GI) peptides on bile secretion and biliary tract mobility, we studied the effects of GI peptides on gallstone formation in guinea pigs fed on low protein lithogenic diet. The peptides under study included cholecystokinin octapeptide (CCK-8), vasoactive intestinal peptide (VIP), somatostatin (SRIF), secretin (SEC), and neurotensin (NT). Hepatic bile flow, electrolytes, and other bile components were also measured. It was found that CCK-8 and VIP suppressed the formation of gallstones and increased hepatic bile flow and Na+, K+, Cl- output significantly. On the other hand, SRIF significantly promoted gallstone formation. The rates of gallstone formation in CCK-8, VIP, and SRIF treated guinea pigs were 15.4%, 23.5%, and 88.0%, respectively, in contrast to 56.8% in the control group. The inhibitory effect of CCK-8 and promoting effect of SRIF on gallstone formation were dose-dependent.
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PMID:Effects of gastrointestinal peptides on formation of gallstone in guinea pigs. 167 24

Cyclic AMP production in response to agonists which act at a variety of receptors to either stimulate or inhibit cyclic AMP production has been studied in intact, dissected ciliary processes from rabbit eyes after unilateral surgical removal of the cervical ganglion. Cyclic AMP responses to stimulatory ligands vasoactive intestinal peptide (VIP), isoproterenol, and forskolin and inhibitory agonists neuropeptide Y (NPY), the synthetic somatostatin analogue SMS 201-995, and alpha-adrenergic agents were investigated in tissues from normal eyes and compared to the same responses in tissues from sympathetically denervated eyes. Neither stimulated cyclic AMP production nor inhibition of stimulated cyclic AMP production was significantly different in tissues from denervated vs. normal eyes. Inhibition of VIP-stimulated cyclic AMP production by epinephrine and paraaminoclonidine in tissues from both normal and denervated eyes was blocked by the alpha 2-adrenergic antagonist yohimbine but not by the alpha 1-adrenergic antagonist prazosin. These data indicate that the VIP, NPY, somatostatin, and alpha 2- and beta 2-adrenergic receptors which regulate cyclic AMP production in rabbit ciliary processes are postjunctional and suggest that ligands known to modulate cyclic AMP levels in this tissue may exert effects on aqueous humor formation independently of adrenergic innervation.
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PMID:Stimulatory and inhibitory cyclic AMP responses in rabbit ciliary processes after cervical ganglionectomy. 167 9

The anterior major pelvic ganglion (AMPG) of the male guinea-pig has been found to consist of three principal components. The presence of a cholinergic component was determined by the demonstration of cytoplasmic and nerve fibre acetylcholinesterase activity. A noradrenergic component was demonstrated by immunoreactivity (IR) of the catecholamine-synthesising enzymes tyrosine hydroxylase (TH) and dopamine-beta-hydroxylase (DBH) in neuronal perikarya. The AMPG also had a peptidergic component which may or may not sub-classify the cholinergic and noradrenergic components. Neuropeptide Y (NPY)-, vasoactive intestinal peptide (VIP)-, and atrial natriuretic factor (ANF)-immunoreactivities were seen in neuronal perikarya, nerve fibres and nerve terminals/varicosities, while somatostatin (SOM)-IR was restricted to neuronal perikarya. Substance P (SP)-IR was present in a dense network of varicose nerve fibres. However, on a rare occasion SP-IR was observed in neuronal perikarya. Enkephalin (ENK)-IR occurred in a sparsely distributed plexus of varicose nerve fibres. The analysis of adjacent serial sections demonstrated distinct patterns of neuropeptide coexistence in AMPG neurons. NPY-IR was colocalised to a subpopulation of TH-IR neuronal perikarya. NPY-IR was also colocalised with VIP-IR in non-TH-IR neuronal perikarya. VIP-IR occurred together with AChE in particular neuronal perikarya. The relationship between immunoreactive neuronal perikarya and immunoreactive nerve terminals was investigated. SP-IR nerve terminals were closely related to neuronal perikarya exhibiting VIP-, NPY-, or TH-IR. TH-IR neuronal perikarya were also abutted by ENK-IR nerve terminals. VIP- and NPY-immunoreactive neuronal perikarya were abutted by two nerve terminal types: one immunoreactive for VIP, the other for NPY. DBH-IR neuronal perikarya received AChE-positive varicosities while AChE-positive neurons were abutted by DBH-IR varicose nerve fibres. AChE-positive varicosities were also closely related to neuronal perikarya possessing VIP-IR and AChE activity.
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PMID:Specific patterns of immunoreactivity in neuronal elements of the anterior major pelvic ganglion of the male guinea-pig. 168 Aug 42


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