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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 635 (1991), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature 325 (1987), S. 813-816 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Figure 1 illustrates the time course of vasopressin (AVP) and oxytocin (OT) release from isolated nerve terminals in the presence or absence of 10~7 M relaxin. An increase in hormone secretion was induced by depolarizing the isolated nerve terminals (neurosecretosomes) with 100 mM K+ for 10 min. ...
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  • 3
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Information in neurons flows from synapses, through the dendrites and cell body (soma), and, finally, along the axon as spikes of electrical activity that will ultimately release neurotransmitters from the nerve terminals. However, the dendrites of many neurons also have a secretory role, ...
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  • 4
    ISSN: 1432-1106
    Keywords: Opioid peptides ; Neurohypophysis ; Nerve endings ; Vasopressin ; Oxytocin ; Calcium ; Release ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Rat neural lobes and isolated nerve terminals from the neurohypophysis were stimulated in the presence of different opioid agonists and antagonists. The secretion of arginine vasopressin and oxytocin and rise in cytoplasmic calcium induced by depolarization were analyzed by radioimmunoassay and the fluorescent probe fura-2, respectively. The kappa-agonists dynorphin A1 -13 and dynorphin A1 -8 did not affect electrically evoked release of vasopressin, although oxytocin release was slightly reduced. U-50 488, a relatively specific kappa-receptor agonist, had no effect on the amount of vasopressin or oxytocin secreted, although it significantly reduced K+-evoked changes in [Ca2+]i in isolated nerve endings. Two kappa-receptor antagonists, MR 2266 and diprenorphin, alone had no effect on vasopressin and oxytocin secretion from isolated nerve endings depolarized with potassium. Opioid agonists less selective for the kappa receptors, etorphin and ethylketocyclazocin, were found to inhibit the release of both vasopressin and oxytocin significantly. Naloxone, a nonselective opiate receptor antagonist, alone had no effect on vasopressin release but potentiated the electrically evoked release of oxytocin. Naloxone also could overcome the inhibitory effect of etorphin on oxytocin and vasopressin release observed after electrical stimulation of the neural lobe. A number of inconsistencies therefore exist between the effects of opioid agonists and antagonists on neuropeptide release and on the evoked changes in [Ca2+]i. In view of these inconsistencies and the high concentrations of opioid agonists and antagonists necessary to modify release, we conclude that it is doubtful that opioid molecules have a physiological role in controlling neurohypophysial secretion.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1573-9023
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Summary Intracellular Ca2+ concentrations ([Ca2+]i) were measured in single-cultured human epithelial intestinal HT-29-D4 cells by digital microscopy using the Ca2+-sensitive fluorescent dye Fura-2. Exposure of these cells to HIV-1 surface-envelope glycoprotein gp120, or to a soluble form of its precursor (gp160), resulted in a significant, dose-dependent rise in [Ca2+]i. gp120 or gp160 specifically abrogated the [Ca2+]i response to the neuropeptide agonist neurotensin, which is a stimulator of chloride secretion via inositol trisphosphate-mediated Ca2+ mobilization. By contrast, upon exposure to neurotensin gp120 failed to show any increase in [Ca2+]i within the same cells, suggesting that both neurotensin and gp120 stimulate a common pathway of [Ca2+]i mobilization. gp120-/gp160-induced [Ca2+]i responses were abolished by preincubation with neutralizing antibodies directed against the third variable domain of gp120. These antibodies inhibited the binding of gp120/gp160 to galactosylceramide (GalCer), the alternative HIV-1 receptor in HT-29-D4 cells. Furthermore, HT-29-D4 cells displayed an important increase in [Ca2+]i to anti-GalCer mAb alone, which rendered the cells insensitive to gp120. By contrast, HT-29-D4 cells became insensitive to anti-GalCer mAb after exposure to gp120. These data indicate that HIV-1 may directly alter enterocytic functions through interaction with the GalCer receptor.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1573-4935
    Keywords: Neurosecretion ; Vasopressin ; Guanine nucleotides ; G-proteins
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Abstract In SLO-permeabilized isolated nerve endings from the rat neurohypophysis, GTP, guanosine 5′[y-thio]triphosphate (GTPyS) and guanosine 5′(ßy-imido]triphosphate (GMPPNP) inhibit the Ca2+-evoked vasopressin release. Pretreatment with pertussis toxin enhances the inhibitory effects of both GTP-analogues. Omission of Mg2+ overcomes the effect of GMPPNP and reverses the inhibitory effect of GTP and GTPyS. In the absence of Mg2+, GTP and GTPyS now potentiate Ca2+-evoked secretion.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1573-4935
    Keywords: neurosecretion ; nerve endings ; stimulus-secretion coupling ; secretion ; exocytosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Abstract In the present paper we discuss the properties of a recently developed preparation of isolated neurosecretory nerve endings obtained from the rate neurohypophysis. These nerve terminals release two neurohormones, oxytocin and vasopressin, which are easily assayed by radioimmunoassay. Depolarization-induced secretion is dependent on the same parameters as those regulating release from the whole neural lobe. The isolated nerve endings can be permeabilized by means of digitonin; a treatment which gives direct access to the cytoplasm allowing the study of the minimal requirements for inducing neuropeptide release. Furthermore, some nerve endings are large enough to allow the use of the patch-clamp technique. In the present paper we present evidences which show that the isolated neurohypophysial nerve terminals represent a protent tool for studying the mechanism of stimulus-secretion.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Bioscience reports 8 (1988), S. 471-483 
    ISSN: 1573-4935
    Keywords: exocytosis ; secretion ; neuropeptides ; vasopressin ; neurohypophysis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Abstract Neurohypophysial hormones are packed in secretory granules which are stored in nerve endings and in dilatations called nerve swellings. Although it was originally believed that the nerve swellings were storage compartments and that release occurred solely from the nerve terminals, the present paper demonstrates that secretion can occur to the same extent from both nerve endings and nerve swellings.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1432-0878
    Keywords: Vasopressin ; Oxytocin ; Opioid peptides ; Neurosecretion ; Neural lobe ; Co-localization ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary The content of vasopressin, oxytocin, neurophysin, leucine-enkephalin, methionine-enkephalin, dynorphin-(1–13), and α-neoendorphin in the rat neurohypophysis was measured after different periods of dehydration and after depolarisation of isolated neural lobes and of neurosecretory nerve endings. The rates at which the amount of neurohypophysial hormone and opioid peptides decreased, and the changes in the ratios between the amount of vasopressin or oxytocin and opioid peptide in the neurohypophysis after dehydration and in the incubation medium after depolarization in vitro cast some doubt on, and can be explained by mechanisms other than co-localisation of the different peptides.
    Type of Medium: Electronic Resource
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