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 functional role of three putative neurotransmitter systems in the visual cortex is compared; the GABAergic inhibitory interneurons, the interneurones containing somatostatin and the cholinergic input originating from the nucleus basalis of Meynert (nbM). Evidence is presented to support the role of GABAergic processes in the generation of the functional structure of the visual cortex and the view that the cholinergic input exerts a neuromodulatory influence enhancing stimulus selective responses. Although the neuropeptide somatostatin produces facilitatory and inhibitory effects on visual cortical cells there is no clear functional pattern to its action. The possible significance of this data and the interaction of SSt with GABA is discussed in the light of evidence that they may coexist in some cells.
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PMID:Modulatory and inhibitory processes in the visual cortex. 286 40

Immunohistochemical studies with antisera to somatostatin have, in many instances, led the way to our present understanding of the peptidergic nervous system. Somatostatin was among the first of the hypophysiotropic hormones shown to be contained in diverse neuronal circuits outside of the hypothalamus. For example, somatostatin is found within neurons ranging in location from the cerebral cortex to primary sensory neurons to enteric neurons within the gut wall. Somatostatin was also the first neuropeptide demonstrated to coexist within vertebrate neurons that also produce a classical neurotransmitter. Since this initial demonstration in sympathetic ganglionic neurons, somatostatin and numerous other neuropeptides have been demonstrated to coexist with a variety of classical neurotransmitters. The "rules" for coexistence are not clear, since somatostatin coexist in some instances with norepinephrine, in other cases with GABA, and probably with other classical transmitters as well. In some neurons, somatostatin also coexists with certain other neuropeptides. Finally, the specificity of immunohistochemical localizations of somatostatin has now been confirmed by virtue of the co-staining of somatostatin neurons with antisera to other portions of the biosynthetic precursor to somatostatin.
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PMID:Immunocytochemical studies of somatostatin neurons in brain. 286 29

Studies carried out in the years since William Beaumont's direct observations of gastric motility have provided increased understanding of the physiological roles of the stomach and of the mechanisms for the regulation of gastric motility. Tonic contractions of the proximal stomach are of primary importance for transfer of liquids from the stomach to the duodenum. Peristaltic contractions of the distal stomach are of primary importance for reducing the size of solid food particles and for transfer of solids to the duodenum. Because gastric emptying requires a net antral-duodenal pressure gradient, contractions of the duodenum also influence the rate of gastric emptying. Gastrointestinal hormones, including gastrin, cholecystokinin, secretin, somatostatin, and others, are released by contact of chyme with the intestinal mucosa, and affect contractions of the proximal stomach, distal stomach, and duodenum. Neural reflexes that arise from the stomach act through autonomic motor nerves to allow regulation by the central nervous system of gastric motility. gamma-Aminobutyric acid, opioids, and bombesin may serve as central neurochemical regulators of gastric motility.
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PMID:Regulation of gastric emptying. 286 73

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

We examined the effects of cholinergic, peptidergic and GABAergic agents on secretin secretion from canine duodenal mucosal explants incubated in organ culture media. Carbachol (10(-12) to 10(-4) M), atropine (10(-6) to 10(-4) M), hexamethonium (10(-6) to 10(-4) M), and somatostatin did not alter basal secretion of secretin. Somatostatin (10(-7) to 10(-8) M) inhibited secretin secretion stimulated by pH 4.5. Met, Leu and their D-ala2-analogs inhibited both basal and pH 4.5-stimulated secretin. Naloxone reversed the inhibition caused by met-enkephalin at pH 7.4. GABA (10(-9) to 10(-6) M) stimulated both basal and pH 4.5-stimulated secretin secretion. GABA-stimulated secretin secretion was neuronal in nature, bicuculline sensitive and was mediated via post ganglionic cholinergic neurons. GABA-stimulated secretin secretion was inhibited by both somatostatin and metenkephalin, suggesting that GABA-stimulated secretin secretion may be under the inhibitory control of peptidergic agents as well.
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PMID:Neurohormonal regulation of secretin secretion in canine duodenal mucosa in vitro. 287 46

gamma-Aminobutyric acid (GABA) is found in high concentrations in the pancreatic islet. In addition, enzymes regulating the level of GABA (L-glutamate decarboxylase and GABA-alpha-ketoglutarate transaminase) have been immunohistochemically localized in the medullary cells of the islet. In this study, an immunofluorescence and elution/restaining protocol is used to determine the distribution of GABA and either insulin, glucagon, or somatostatin in a tissue section. GABA was not detected within the islet alpha- or delta-cells but was determined to be localized within the insulin-containing beta-cells.
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PMID:Immunohistochemical colocalization of GABA and insulin in beta-cells of rat islet. 287 11

While the dentate gyrus is clearly the simplest of the cortical fields that constitute the hippocampal formation, it nonetheless occupies a pivotal position in the flow of information through this region. Though it has been the subject of anatomical study for over a century and its major connections have been known for almost as long, the use of newly developed histochemical and immunohistochemical techniques have demonstrated many new facets of its intrinsic connectivity and afferent innervation. These techniques have established that it is innervated by cholinergic, noradrenergic, serotonergic and dopaminergic fibers. More recent studies have shown that fibers and cell bodies of the dentate gyrus are immunoreactive for variety of neuroactive substances including the excitatory amino acids glutamate and aspartate, the inhibitory transmitter GABA, as well as peptides of many types including the opioid peptides, enkephalin and dynorphin, several forms of somatostatin, neuropeptide Y, cholycystokinin, vasoactive intestinal peptide and substance P. In this review, we will briefly summarize the distribution of each of these putative transmitter systems within the dentate gyrus. The perspective emerges that the plethora of newly identified and chemically specific fiber systems enriches the classical understanding of the organization of this relatively simple cortical structure. Since there is thus far no evidence for the exclusion from the dentate gyrus of any class of transmitter bearing fiber or neuron found in the neocortex, it can be viewed as a relatively simple model system for studying the interactions of specific transmitter systems in a laminated, cortical structure.
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PMID:Transmitter systems in the primate dentate gyrus. 287 75

CSF neurotransmitter markers may reflect neurochemical alterations in Alzheimer's disease (AD). The best studied neurochemical deficit in AD is that of acetylcholine. Both acetylcholinesterase and butyrylcholinesterase activity have been reported to be reduced in some but not all studies of AD CSF. Studies of monoamine metabolites have also been controversial but most authors have found reduced concentrations of CSF HVA, lesser reductions in HIAA and no change in MHPG. CSF GABA concentrations have been found to be reduced in AD. Studies of CSF neuropeptides in AD have shown reduced concentrations of somatostatin and vasopressin, normal concentrations of vasoactive intestinal polypeptide and either normal or decreased concentrations of beta-endorphin and corticotropin releasing factor. Although no individual CSF neurochemical markers are specific for AD it may be possible to develop a profile of several neurochemical markers which will have enhanced specificity.
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PMID:CSF neurotransmitter markers in Alzheimer's disease. 287 17

A [K+]-related, Ca2+-dependent efflux of immunoreactive somatostatin (IRS) from superfused slices of rat cerebral cortex has been observed; this release paralleled the release of both [14C]noradrenaline and [14C]GABA. However IRS release in this preparation was not stimulated by the muscarinic agonist carbachol at low (10 microM) or high (500 microM) concentrations. Furthermore, 100 or 500 microM carbachol did not affect the IRS efflux from rat cortex slices incubated in the presence of 12, 25 or 53 mM K+.
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PMID:Failure of carbachol to influence the release of somatostatin from slices of rat cerebral cortex. 287 3

The chicken retina has been used to examine the toxicity of a highly reactive chemical analog of choline, ethylcholine mustard aziridinium ion (ECMA). Following a single intravitreal injection, retinas were analyzed biochemically for CAT and AChE activities, and GABA, glycine, and dopamine levels. Retinas were also examined using histofluorescence for dopamine histochemistry, for AChE, and immunohistochemistry with antibodies to CAT, tyrosine hydroxylase, GABA, 5-HT, Leu-enkephalin, and somatostatin. A dose of 50 nmol ECMA caused a prolonged 70% depletion of CAT activity and a 40% depletion of AChE activity. The other biochemical parameters were unchanged. This result corresponds to the morphological finding that 2 populations of cholinergic cells were destroyed and that the AChE activity associated with their terminal arbors was lost. A third population of cholinergic cells, located towards the middle of the inner nuclear layer, was resistant to the toxic effects of ECMA. The other cell types, except for somatostatin-immunoreactive cells and photoreceptors, which showed transient effects, were unaffected. ECMA therefore appears to be a highly specific toxin for cholinergic cells in the retina.
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PMID:The toxic effects of ethylcholine mustard aziridinium ion on cholinergic cells in the chicken retina. 288 Sep 36


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