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  • 1
    Electronic Resource
    Electronic Resource
    Serotonin Binding Protein: Synthesis, Secretion, and Recycling (1994)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 63 (1994), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Serotonin binding protein (SBP) is present in all neurectodermally derived cells that store serotonin (5-HT). Three forms of SBP have been detected (68, 56, and 45 kDa), and antibodies to SBP that interfere with the binding of 5-HT react with each of these proteins. The current experiments test two hypotheses: (a) that the 56- and 45-kDa forms of SBP are produced by posttranslational cleavage of a 68-kDa precursor molecule; and (b) that 45-kDa SBP is a constituent of serotonergic secretory vesicles. Pulse-chase experiments were carried out using medullary thyroid carcinoma cells as a model. These neurectodermally derived cells produce 5-HT and all three forms of SBP. Following pulse labeling for 20 min with l-[35S]methionine, the cells were incubated in the presence of an excess of unlabeled l-methionine for 0, 30, 60, or 90 min at 37°C. Alternatively, the chase was performed under conditions (20°C, inhibition of ATP generation) that delay or stop transport of newly synthesized proteins from the rough endoplasmic reticulum through the Golgi apparatus. Following incubation, the cells were washed and solubilized, and SBP was immunoprecipitated. Radioactive proteins in the immunoprecipitate were electrophoretically resolved and quantified. Immediately after the pulse, each of the three forms of SBP was found to be labeled with 35S. The relative proportions of 35S-labeled 68-, 56-, and 45-kDa SBP remained the same at each interval of chase. These proportions were not changed when the chase was carried out at 20°C or under conditions that blocked the biosynthesis of ATP. These observations suggest that each form of SBP is a primary product of translation, that the smaller forms of SBP are not produced by cleavage from a larger molecule, and that the size of the primary products of translation is not altered by passage to the Golgi apparatus or a post-Golgi compartment. When secretion was induced, 45-kDa SBP, but not 56- or 68-kDa SBP, was released to the medium. When antibodies to 45-kDa SBP were added to the medium at the time secretion was induced, antibody binding sites appeared as patches on the cell surfaces. Because of these sites, cells were lysed when they were stimulated to secrete in the presence of antibodies to 45-kDa SBP and guinea pig complement. Antibody binding sites disappeared from cell surfaces after 20 min, at which time antibodies to SBP were found inside the cells. It is suggested that 45-kDa SBP is packaged with 5-HT in secretory vesicles. Some 45-kDa SBP is lost during secretion as a result of exocytosis; however, a fraction of the 45-kDa SBP remains bound to the luminal surface of the membrane of secretory vesicles. This protein is exposed to the ambient medium as a consequence of exocytosis, but is reinternalized when the vesicular membrane is recaptured during vesicle recycling.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1994.63010097.x
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  • 2
    Electronic Resource
    Electronic Resource
    Identification of Serotonin Receptors Recognized by Anti-Idiotypic Antibodies (1991)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 57 (1991), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Anti-idiotypic antibodies were generated by immunizing rabbits with affinity-purified antibodies to serotonin (5-hydroxytryptamine; 5-HT). Anti-5-HT activity was removed from the resulting antisera by chromatography through a 5-HT affinity column. The anti-idiotypic antibodies were demonstrated by enzyme-linked immunosorbent assay to bind to affinity-purified whole anti-5-HT antibodies and their Fab fragments. Anti-idiotypic antibodies, purified by affinity chromatography on columns to which antibodies to 5-HT were coupled, competed with 5-HT (covalently bound to protein) for the binding sites on anti-5-HT antibodies and serotonin binding protein. The anti-idiotypic antibodies antagonized the binding of [3H]5-HT to membranes isolated from the cerebral cortex, striatum, and raphe area more than to membranes from hippocampus or cerebellum. The anti- idiotypic antibodies also blocked the binding of the 5-HT1B- selective ligand (-)-[125I]iodocyanopindolol (in the presence of 30 μM isoproterenol) to cortical membranes. In contrast, anti-idiotypic antibodies failed to inhibit binding of the 5- HT1A-selective ligand 8-hydroxy-2-(di-n)-[3H]propylamino)- tetralin ([3H]8-OH-DPAT) to raphe area membranes or hippocampal membranes. These observations suggested that the anti-idiotypic antibodies may recognize some 5-HT receptor subtypes but not others. This hypothesis was tested by ascertaining the ability of anti-idiotypic antibodies to immunostain cells transfected in vitro with cDNA encoding the 5- HT1C or 5-HT2 receptor or with a genomic clone encoding the 5-HT1A receptor. Punctate sites of immunofluorescence were found on the surfaces of fibroblasts that expressed 5- HT1C and 5-HT2 receptors, but not on the surfaces of HeLa cells that expressed 5-HT1A receptors. Immunostaining of cells by the anti-idiotypic antibodies was inhibited by appropriate pharmacological agents: immunostaining of cells expressing 5-HT1C receptors was blocked by mesulergine (but not ketanserin, 8-OH-DPAT. or spiperone), whereas that of cells expressing 5-HT2 receptors was blocked by ketanserin or spiperone (but not mesulergine or 8-OH-DPAT). The anti- idiotypic antibodies failed to inhibit the uptake of [3H]5-HT by serotonergic neurons. It is concluded that the anti-idiotypic antibodies generated with anti-5-HT serum recognize the 5- HT1B, 5-HTlC, and 5-HT2 receptor subtypes; however, neither 5-HT1A receptors nor 5-HT uptake sites appear to react with these antibodies.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1991.tb08240.x
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  • 3
    Electronic Resource
    Electronic Resource
    Serotonin-Storing Secretory Vesicles (1990)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 600 (1990), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1990.tb16872.x
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  • 4
    Electronic Resource
    Electronic Resource
    Distribution of laminin in the murine pituitary (1990)
    New York, NY [u.a.] : Wiley-Blackwell
    The @Anatomical Record 226 (1990), S. 471-480 
    Details
    ISSN: 0003-276X
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: The distribution and cellular localization of the glycoprotein laminin were investigated by light and electron microscopic immunocytochemistry in the adult murine pituitary gland. Immunoblots confirmed that laminin was the only protein in the pituitary gland of the adult male mouse to react with antilaminin serum. Laminin immunoreactivity was demonstrated at the light microscopic level simultaneously with that of β-follicle stimulating hormone (β-FSH) and β-luteinizing hormone (β-LH). In addition to its distribution is basal laminae, laminin immunoreactivity was coincidently expressed in gonadotrophs with the immunoreactivities of β-FSH and β-LH. Electron microscopic immunocytochemistry was employed on aldehyde-fixed sections embedded in L.R. White. Sites of binding of primary antisera to laminin were identified with affinity-purified secondary antisera directly coupled to 20 nm particles of colloidal gold. Three antisera recognizing laminin were compared and found to result in an identical pattern of immunoreactivity. Laminin was found extracellulary only in formed basal laminae in all three lobes of the pituitary and was not found in extracellular matrices of connective tissue. Laminin immunoreactivity was also found intracellularly in gonadotrophs but in none of the other endocrine or non-endocrine cells of the anterior lobe. Within gonadotrophs, only secretory granules were labeled. The majority, but not all, secretory granules were labeled in each of the gonadotrophs examined, and the proportion of granules labeled with laminin could not be increased by doubling the concentration of anti-laminin serum. Laminin immunocreactivity segregated with the subset of secretory granules containing β-FSH. In contrast, laminin immunoreactivity was absent in the smaller subset of secretory granules that contain serotonin. No secretory granules were labeled within the endocrine cells of the intermediate lobe, nor within secretory granules of neural elements in the posterior lobe.
    Additional Material: 8 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/ar.1092260409
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  • 5
    Electronic Resource
    Electronic Resource
    Role of growth factors in catecholaminergic expression by neural crest cells: In vitro effects of transforming growth factor beta1 (1993)
    New York, NY [u.a.] : Wiley-Blackwell
    Developmental Dynamics 196 (1993), S. 1-10 
    Details
    ISSN: 1058-8388
    Keywords: Chick embryo extract-derived factors ; Catecholaminergic phenotypic expression ; Neural crest-derived cells ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: The differentiation of neural crest cells into catecholaminergic neurons is dependent upon both intrinsic properties and signals from the embryonic microenvironment. In tissue culture, the development of catecholaminergic traits is dependent upon factors present in chick embryo extract (CEE). This dependency suggests that soluble growth factors affect catecholaminergic differentiation in vivo. We have studied the role of CEE-derived factors and the potentially related influence of characterized growth factors on catecholaminergic phenotypic expression in avian neural crest cells. In this report, we show that CEE-derived factors and transforming growth factor beta1 (TGF-β1) differentially influence catecholaminergic phenotypic expression as well as melanogenesis. TGF-β1 substituted for CEE-derived factors and supported the in vitro differentiation of tyrosine hydroxylase (TH) and dopamine-β-hydroxylase (DBH) immunoreactivities, as well as catecholamine biosynthesis and storage. Differentiation of catecholaminergic cells was dependent on factors present in 10% CEE during the first 1-4 days in culture suggesting an initial critical period for exposure. One day of initial exposure to either CEE-derived factors or TGF-β1 was sufficient to support the subsequent expression of catecholaminergic phenotypic characteristics. The time course of responsiveness to TGF-β1 was different than for CEE-derived factors. Neural crest cells remain responsive to TGF-β1 for at least 5 days, which is past the critical period for CEE-derived factors. Bioassay of CEE shows that endogenous levels of TGF-β are less than or equal to 0.5 ng/ml. Immunoprecipitation of TGF-β from CEE or blockade by neutralizing antibodies did not result in a loss of catecholaminergic differentiation by neural crest cells. Although CEE supports melanogenesis under all of the growth conditions tested, TGF-β1 was found to be inhibitory. © 1993 wiley-Liss, Inc.
    Additional Material: 3 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/aja.1001960102
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  • 6
    Electronic Resource
    Electronic Resource
    Colonization of the bowel by neural crest-derived cells re-migrating from foregut backtransplanted to vagal or sacral regions of host embryos (1993)
    New York, NY [u.a.] : Wiley-Blackwell
    Developmental Dynamics 196 (1993), S. 217-233 
    Details
    ISSN: 1058-8388
    Keywords: Neural Crest ; Neural Crest Migration Pathways ; Quail-Chick Chimeras ; Developing Bowel ; Back-Transplantation ; Enteric Nervous System ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: The enteric nervous system (ENS) in avian embryos is formed by cells that migrate to the bowel from vagal and sacral regions of the neural crest. Experiments were carried out to evaluate the developmental potential of crest-derived cells at the time they colonize the gut. Backtransplantation of E4 quail foregut (or control aneuronal hindgut) was used to determine whether crest-derived cells that have previously colonized the bowel are capable of following defined neural crest migration pathways in host embryos. Vagal and sacral, but not truncal, backgrafts provided donor cells for the host's bowel. These cells were immunostained by the neural crest marker, NC-1, restricted to the ENS, and appeared only when foregut was backgrafted; therefore, they were crest-derived. In order for cells to migrate to the host's bowel, backgrafts evidently had to be located in the vicinity of the neuraxis at the time crest-derived cells exited from them. When vagal grafts moved away from the neuraxis, crest-derived donor cells colonized cephalic ganglia and the vagus nerves near the grafts; however, such cells did not migrate down the vagi to the host's gut. Sacral backgrafts provided crestderived cells for the bowel only if the donor gut was transplanted prior to the formation of somite 28, at the level of the disappearing primitive streak. Cells from vagal backgrafts were capable of reaching the host's cloaca, but backgrafts placed at a sacral level colonized only the postumbilical bowel. In addition, donor cells proliferated extensively within the host's gut. Whenever the host's gut was colonized, donor crest-derived cells were also found in non-enteric targets including nerves, cephalic (vagal backgrafts), or sympathetic (sacral backgrafts) ganglia; however, donor cells did not form ectomesenchyme or melanocytes. These data suggest that (i) crest-derived cells that have colonized the bowel remain capable of remigrating and following defined neural crest migration pathways in host embryos; (ii) remigrating cells must enter these pathways at their start; (iii) the gut stimulates the proliferation of enteric crest-derived cells; (iv) vagal crest-derived cells can follow sacral pathways to reach enteric, Remak's, or sympathetic ganglia; and (v) the migration of crest-derived cells within the gut is determined more by the route they follow to reach the bowel than by their level of origin in the neural crest. © 1993 wiley-Liss, Inc.
    Additional Material: 9 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/aja.1001960308
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  • 7
    Electronic Resource
    Electronic Resource
    Structural abnormalities associated with congenital megacolon in transgenic mice that overexpress the Hoxa-4 gene (1993)
    New York, NY [u.a.] : Wiley-Blackwell
    Developmental Dynamics 198 (1993), S. 28-53 
    Details
    ISSN: 1058-8388
    Keywords: Enteric nervous system ; Peripheral nervous system ; Neural crest ; Mutant mice ; Congenital megacolon ; ls/ls mice ; Homeobox genes ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: Congenital megacolon develops in transgenic mice that overexpress the homeobox-containing gene, Hoxa-4. The current study was done to identify abnormlities of the terminal colon that might account for the phenotype. The terminal bowel of transgenic mice was compared with that of control and lethal spotted (ls/ls) mice, a strain in which megacolon also develops. The terminal colon of the transgenic mice contained fewer ganglia than that of controls, but was hypoganglionic, rather than aganglionic like that of ls/ls mice. The neurons present in the adult transgenic colon were sifnificantly increased in size and a subset of very large neurons(〉40 μm in maximum diameter) were observed. Electron microscopic studies of young adult transgenic mice revealed that the ganglia and nerves of the myenteric plexus had the ultrastructure of extraenteric peripheral nerve rather than that of the enteric nervous system (ENS). The myenteric ganglia in the transgenic animals contained Schwann cells associated with a basal lamina that enveloped axons completely and individually, instead of glia. Although collagen is excluded from the ganglia and thin nerve fibers of the normal ENS, a collagen-containing endoneurium surrounded each of the axon-Schwann cell units of the abnormal nerve fibers of the transgenic mice were located in these nerve bundles rather than in ganglia. There were smooth muscle abnormalities in the terminal bowel of the transgenic mice. Wide gaps were present in the longitudinal muscle of the transgenic mice; these gaps contained ganglia that were in contact with the adventitia. These longitudinal smooth muscle cells were more irregular than those of controls and they contained fewer puncta adherens; moreover, a larger proportion of the volume of the cytoplasm of transgenic smooth muscle cells was occupied by organelles. Finally, an extensive thickening and reduplication of the basal lamina surrounding the smooth muscle cells of the muscularis mucosa was observed in the transgenic colon and resembled that found in ls/ls mice. These data suggest that both smooth muscle and the innervation of the terminal bowel of neonatal Hoxa-4 transgenic mice are structurally abnormal. Although some of the abnormalities seen in Hoxa-4 transgenic mice are similar to those which arise in ls/ls mice, the two conditions are not identical. In both animals, the data are consistent with the hypothesis that the defects arise as a result of a defective interaction between the precursors of enteric neurons and smooth muscle. © 1993 Wiley-Liss, Inc.
    Additional Material: 15 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/aja.1001980105
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