UNIPROT:P61278 - FACTA Search

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Query: UNIPROT:P61278 (somatostatin)
22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Striatal atrophy in Huntington's disease (HD) is characterized by selective preservation of a subclass of neurons colocalizing NADPH-diaphorase (NADPH-d), somatostatin (SS), and neuropeptide Y (NPY), which have been reported to show three- to fivefold increases in SS-like immunoreactivity (SSLI) and NPY content. Since HD brain is capable of producing excessive quantities of the excitotoxin quinolinic acid (Quin), an N-methyl-D-aspartate (NMDA) receptor agonist, and since experimental Quin lesions show neuronal loss with sparing of NADPH-d/SS/NPY neurons, it has been suggested that Quin may be important in the pathogenesis of HD. In the present study we determined whether Quin stimulates SS gene function in cultured cortical cells known to be rich in NADPH-d/SS/NPY neurons. Cultures of dispersed fetal rat cortical cells were exposed to Quin (1 and 10 mM) with or without (-)-2-amino-5-phosphonovaleric acid (APV; 0.5 mM), an NMDA receptor antagonist, NMDA (0.2 and 0.5 mM), and glutamate (Glu; 0.5 mM). Medium and cellular SSLI was determined by radioimmunoassay and SS mRNA by Northern analysis with a cRNA probe. Quin induced significant (p less than 0.01) 1.6- and 2.5-4 fold increases in SSLI and SS mRNA accumulation, respectively, which were abolished by APV. Release of SSLI into the culture medium was stimulated two- to fivefold by Quin over a 2- to 20-h period. The increase in SS mRNA produced by Quin was time and dose dependent. A similar dose-dependent increase in SS mRNA comparable with that observed with Quin was induced by NMDA.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Quinolinic acid stimulates somatostatin gene expression in cultured rat cortical neurons. 167 45

The localization and distribution of somatostatin and neuropeptide Y were studied in the porcine female reproductive system with the indirect immunofluorescence technique. Somatostatin-immunoreactive nerve fibers were observed in different parts of the ovary and in the muscular membrane of the uterus as well as in the mesosalphinx. Somatostatin-immunoreactive neurons were detected in the inferior mesenteric ganglion. Neuropeptide Y immunoreactivity was present in a large number of nerve fibers distributed in different regions of the uterus, oviduct and ovary. The present results suggest that the porcine female genital organs receive innervation by somatostatin- and neuropeptide Y-containing nerve fibers, but their exact functional role remains to be established.
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PMID:Distribution of somatostatin- and neuropeptide Y-immunoreactive nerve fibers in the porcine female reproductive system. 167 21

The effects of aging on inhibitory neuropeptide concentrations and intrinsic inhibitory innervation of circular muscle were investigated using normal descending colon obtained at surgery. Immunoreactive vasoactive intestinal peptide, peptide histidine-methionine, met5-enkephalin, neuropeptide Y, and somatostatin were extracted from specimens of muscularis externa (patient ages: 19-84 years) and measured by radioimmunoassay. Intracellular electrical activity was recorded from strips of circular muscle (patients ages: 49-84 years) using glass microelectrodes; inhibitory junction potentials were evoked by electrical field stimulation. There were no significant differences (t tests: P greater than 0.05) between neuropeptide concentrations in patients less than 70 years old (N = 28) compared to patients greater than or equal to 70 years old (N = 12). However, the amplitude of inhibitory junction potentials declined with increasing patient age (r = -0.58, P = 0.02, N = 16), with no change in resting membrane potentials (r = 0.22; P greater than 0.05). The decline in amplitude in women (r = -0.68, P = 0.03, N = 9) preceded the decline in men (r = -0.62, P = 0.10, N = 7). Age-related decline in inhibitory junction potentials could be related to decreased: density of inhibitory nerves, release of inhibitory neurotransmitter, density of binding sites for inhibitory neurotransmitter on smooth muscle, or a combination thereof. Alternatively, this decline might represent a change in interaction of inhibitory neurotransmitter with the smooth muscle membrane, such as a change in coupling of binding site with the potassium channel, decreased number of potassium channels, or altered permeability of the potassium channel.
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PMID:Inhibitory neuropeptides and intrinsic inhibitory innervation of descending human colon. 167 67

Immunohistochemistry on tissues of larval lampreys, Petromyzon marinus L., was used to determine the distribution of invariant somatostatin-14 (SST-14) and lamprey somatostatin-34 (SST-34) in the brain while antisera against porcine peptide tyrosine tyrosine (PYY), human neuropeptide Y (NPY), anglerfish peptide YG (aPY), salmon glucagon-like peptide (GLP), SST-14, and SST-34 were used in studies of the pancreas and anterior intestine. In the brain, SST-14 is the major form of somatostatin. SST-14- and SST-34-immunoreactive nerve fibers are distributed throughout the telencephalon, diencephalon, and mesencephalon. In the latter region SST-14 immunoreactivity is concentrated in nerve tracts in the nucleus interpeduncularis. Nerve cells within the olfactory bulbs are immunoreactive only to anti-SST-34. Cells immunostained with anti-SST-14 were localized within the ependymal and subependymal layers of the pars ventralis hypothalami and the subependymal layers of the pars dorsalis thalami. SST-14-immunoreactive perikarya are also distributed within the tegmentum mesencephali. Nerve fibers and cells immunoreactive to anti-SST-34 are detected in the pars ventralis hypothalami but these cells do not colocalize SST-14. Pancreatic islets, distributed within the epithelium and in the submucosal connective tissue at the esophageal-intestinal junction, are only immunoreactive to anti-insulin. The antisera revealed three distinct cell types in the intestinal epithelium: type 1 colocalizes aPY, NPY, and PYY; type 2 colocalizes SST-14 and SST-34; and type 3 demonstrates immunoreactivity only to anti-SST-34. Immunoreactivity to anti-GLP is absent.
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PMID:Distribution of two forms of somatostatin and peptides belonging to the pancreatic polypeptide family in tissues of larval lampreys, Petromyzon marinus L.: an immunohistochemical study. 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

Indirect immunocytochemistry of striatal neurons in primary culture, generated from the embryonic mouse brain, suggested that 2-4% of the neurons contained somatostatin-like immunoreactivity; the majority of these cells also contained neuropeptide Y immunoreactivity, characteristic of a subset of striatal interneurons. Although 10-15% of cultured striatal neurons showed moderate or intense immunoreactivity for calbindin-D28k, the majority of neurons with somatostatin-like immunoreactivity did not contain calbindin-D28k-like immunoreactivity; parvalbumin immunoreactivity was absent from the culture preparation. A highly sensitive radioimmunoassay was used to examine the actions of depolarizing agents and excitatory amino acids on the release of endogenous somatostatin-like immunoreactivity from striatal interneurons. During a 15 min incubation period, 47 +/- 10 fmol of somatostatin-like immunoreactivity were released from 14 days in vitro striatal neurons, cultured in 35 mm dishes. Depolarization with 56 mM KCl or 10 micrograms/ml veratrine resulted in an additional 105 +/- 9 and 56 +/- 5 fmol, respectively, of somatostatin-like immunoreactivity released; the release evoked by veratrine was blocked by 1 microM tetrodotoxin. In the presence of 100 microM N-methyl-D-aspartate, 112 +/- 21 fmol of somatostatin-like immunoreactivity (above basal) were released (+238%); the N-methyl-D-aspartate-evoked release was dose-dependent (EC50, 20 microM), attenuated in the absence of added Ca2+, potentiated in the absence of added Mg2+ and unaffected by the presence of 1 microM tetrodotoxin. The selective antagonists 2-amino-5-phosphonovalerate (100 microM) and MK-801 (1 microM) blocked the N-methyl-D-aspartate-evoked release of somatostatin-like immunoreactivity; KCl-evoked release was unaffected. Kainate was slightly more effective, yet five-fold less potent (EC50, 100 microM), than N-methyl-D-aspartate in evoking somatostatin-like immunoreactivity release; quisqualate was marginally effective. The results of this study suggest that N-methyl-D-aspartate and kainate receptors are present on striatal somatostatinergic interneurons in primary culture.
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PMID:N-methyl-D-aspartate evokes the release of somatostatin from striatal interneurons in primary culture. 168 66

By means of double immunolabeling procedures it has been possible to demonstrate glucocorticoid receptor (GR) immunoreactivity (IR) in large numbers of various peptidergic neurons of the brain including neurons containing gastrointestinal peptides, opioid peptides, and peptides with a hypothalamic hormone function. For each peptide system, however, marked heterogeneities exist among brain regions. Thus, in the neocortex and the hippocampal formation most of the brain peptide neurons lack GR IR, while the same types of peptide neurons in the arcuate and paraventricular nucleus [e.g. neuropeptide Y (NPY), somatostatin (SRIF) and the cholecystokinin (CCK) neurons] possess strong GR IR. Furthermore, in the arcuate, parvocellular part of the paraventricular nuclei and the central amygdaloid nucleus practically all the peptidergic neurons are strongly GR IR, while in the lateral hypothalamus, mainly the neurotensin (NT) and galanin (GAL) IR neurons are GR IR. These marked differences among areas probably reflect functional differences dependent upon their participation in stress regulated circuits. All the paraventricular NT, corticotropin-releasing factor (CRF), growth hormone-releasing factor (GRF), thyrotropin-releasing hormone (TRH) and SRIF IR neurons appear to contain GR IR, while the luteinizing hormone-releasing hormone (LHRH) IR neurons lack GR IR, underlying the importance of glucocorticoids (GC) in controlling endocrine function. Finally, the GC may influence pain and mood control mainly via effects on enkephalin (ENK) neurons especially in the basal ganglia (mood) and on all beta-endorphin (beta-END) neurons of the arcuate nucleus, while most of the dynorphin neurons are not directly controlled by GC.
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PMID:Central peptidergic neurons as targets for glucocorticoid action. Evidence for the presence of glucocorticoid receptor immunoreactivity in various types of classes of peptidergic neurons. 168 65

Although it seems highly likely that mammalian isocortex evolved from a structure resembling reptilian telencephalic cortex, it has been uncertain if this occurred by the laminar differentiation of three-layered reptilian cortex into six-layered mammalian isocortex without the addition of new cell types or by laminar differentiation with the addition of new cell types. To distinguish between these two possibilities, immunohistochemical techniques were used to study turtles to see if the same major neuronal cell types, as defined by neurotransmitter or neuropeptide content, present in mammalian isocortex are also present in the specific part of reptilian cortex thought to be the forerunner of at least parts of isocortex, namely the dorsal cortex. Neurons containing the following substances are the major transmitter-specific types of neurons known to be present in mammalian isocortex: cholecystokinin-8 (CCK8), vasoactive intestinal polypeptide (VIP), acetylcholine, substance P (SP), neuropeptide Y (NPY), somatostatin (SS), LANT6, enkephalin, GABA and glutamate (GLUT). In turtles, only those of the above substances that are found in large numbers of neurons in layers V-VI in mammalian isocortex, irrespective of whether they are also present in layers II-IV (i.e. SP, NPY, SS, LANT6, GABA and GLUT), were present in neurons in dorsal cortex. The neurons containing these substances in dorsal cortex in turtles were generally highly similar in morphology to their counterparts in mammalian isocortex. In contrast, neurons labeled for CCK8, VIP or acetylcholine, which are mainly found in neurons of layers II-IV of mammalian isocortex, were absent or extremely rare in dorsal cortex. The absence or paucity of neurons labeled for these latter substances in dorsal cortex in turtles did not reflect an overall staining failure of the antisera used since the same antisera yielded excellent labeling of neurons, fibers and terminals in many other brain regions in turtles. Thus, dorsal cortex in turtles appears to lack several of the major cell types characteristic of layers II-IV of mammalian isocortex, but possesses a number of the major cell types characteristic of layers V-VI of isocortex. The findings support and extend a previous suggestion by Ebner [1976], based on hodological data, that dorsal cortex in turtles may lack the types of neurons found in the more superficial layers of mammalian isocortex.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:A comparison of neurotransmitter-specific and neuropeptide-specific neuronal cell types present in the dorsal cortex in turtles with those present in the isocortex in mammals: implications for the evolution of isocortex. 168 5

We have previously reported a reduction in the inhibitory effect of somatostatin on adenylyl cyclase activity in the superior temporal cortex of a group of Alzheimer's disease cases, compared to a group of matched controls. In the present study, the levels of high affinity 125I-Tyr11-somatostatin-14 binding, its modulation by guanine nucleotides and the effects of somatostatin on adenylyl cyclase activity have been measured in preparations of frontal cortex, hippocampus, caudate nucleus and cerebellum from the same patient and control groups. A significant reduction in 125I-Tyr11-somatostatin-14 binding was observed in the frontal cortex, but not other regions, of the Alzheimer's disease group, compared with control values. The profiles of inhibition of specific 125I-Tyr11-somatostatin-14 binding by Gpp(NH)p were similar in all regions in both groups. No significant differences in basal, forskolin-stimulated, or somatostatin and neuropeptide Y inhibitions of adenylyl cyclase activity were found between the two groups. The pattern of change of somatostatin binding in the Alzheimer's disease cases observed in the present study differs from the reported pattern of loss of somatostatin neurons and may be secondary to the degeneration of somatostatin receptor-bearing cholinergic afferents arising from the nucleus basalis. The results of this study indicate that impaired somatostatin modulation of adenylyl cyclase is not a global phenomenon in Alzheimer's disease brain and also that there are no major disruptions of somatostatin receptor-G-protein coupling or of adenylyl cyclase catalytic activity in this disorder.
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PMID:Regional distribution of somatostatin receptor binding and modulation of adenylyl cyclase activity in Alzheimer's disease brain. 168 16

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