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  • 1
    Online Resource
    Online Resource
    Cham :Springer International Publishing AG,
    Keywords: Neurosciences. ; Electronic books.
    Type of Medium: Online Resource
    Pages: 1 online resource (318 pages)
    Edition: 1st ed.
    ISBN: 9783030229894
    Series Statement: Masterclass in Neuroendocrinology Series ; v.8
    DDC: 612.79999999999995
    Language: English
    Note: Intro -- Series Preface -- Volume Preface -- Contents -- Contributors -- 1: Neurosecretion: A Historical Overview -- 1.1 Introduction -- 1.2 Origin of the Concept of Neurosecretion and the Advent of Neuroendocrinology -- 1.3 Invertebrate and Vertebrate Neurosecretory Systems as Experimental Models -- 1.4 The Biosynthesis of Oxytocin and Vasopressin: A Critical Role for NSVs -- 1.5 Concluding Remarks -- Key References: See Main List for Reference Details -- References -- 2: Neurosecretion: Hypothalamic Somata versus Neurohypophysial Terminals -- 2.1 Introduction -- 2.2 The Hypothalamic-Neurohypophysial System (HNS) -- Box 2.1 Loose Patch-Clamp on NH Terminals (NHTs) versus MCNs -- 2.2.1 Depolarization-Secretion Coupling (DSC) -- 2.3 Magnocellular Neurons -- 2.3.1 VGCC Regulation of Depolarization-Secretion Coupling in Somatodendrites -- 2.3.2 Autocrine Regulation of Magnocellular Neurons by Somatodendritic Release of AVP/OT -- 2.3.3 [Ca2+]i Homeostasis and [Ca2+]i Clearance Mechanisms in the Somatadendrites of AVP and OT Neurons -- 2.3.4 [Ca2+]i Oscillations in the Somata of AVP and OT Neurons -- Box 2.2 Measurements of [Ca2+]i and Spontaneous Calcium Oscillations in MCNs -- 2.3.5 Mechanism for Facilitation of Release in Cell Bodies -- 2.4 Neurohypophysial Nerve Terminals -- 2.4.1 VGCC Regulation of Depolarization-Secretion Coupling in Terminals -- 2.4.2 Autocrine Regulation of Terminals by Release of AVP/OT? -- 2.4.3 Mechanisms of Cytosolic [Ca2+]i Increases in Terminals -- Box 2.3 Measuring Intracellular Ca2+ in NH Terminals (NHTs) -- 2.4.4 Terminals Utilize RyR in Neurosecretory Granules (NSG) to Regulate OT Release -- 2.4.5 Mechanisms of Cytosolic [Ca2+]i Clearance in Terminals -- 2.4.6 Role of Vesicular Ca2+ Stores -- 2.4.7 Mechanism for Facilitation of Release in Terminals -- 2.4.8 Trafficking of NSG Between Release Pools. , 2.4.9 SNARE-Mediated Exocytosis in Somata versus Terminals -- Box 2.4 SNARE-Mediated Fusion in Reconstituted System -- 2.5 Conclusions -- Key References: See Main List for Reference Details -- References -- 3: Cyclic ADP-Ribose and Heat Regulate Oxytocin Release via CD38 and TRPM2 in the Hypothalamus -- 3.1 Introduction -- Box 3.1 CD38 -- 3.2 [Ca2+]i Increase by cADPR and Heat -- Box 3.2 OT Release from the Whole Hypothalamus -- 3.3 Individual Variation in OT Release from the Isolated Hypothalamus -- Box 3.3 Social Stress -- 3.4 In Vivo OT Release Associated with Hyperthermia Induced by Stress -- Box 3.4 Cerebrospinal Fluid (CSF) Sampling -- 3.5 CD38 and TRPM2 mRNA Expression -- 3.6 Implication of Oxytocin Release for Stress and Autism -- Key References: See Main List for Reference Details -- References -- 4: Somato-Dendritic Secretion of Neuropeptides -- 4.1 Introduction -- 4.2 Magnocellular Neurons -- 4.3 Regulation of Somato-Dendritic Secretion in Magnocellular Neurons -- 4.4 Physiological Functions of Somato-Dendritic Neuropeptide Secretion -- 4.4.1 Autocrine Regulation of Vasopressin Neuron Activity -- Box 4.1 In Vivo Extracellular Single-Unit Recording from the Supraoptic Nucleus with Microdialysis Drug Application in Anesthe... -- 4.4.1.1 Autocrine Regulation of Vasopressin Neuron Activity by Co-released Neurotransmitters -- 4.4.2 Paracrine Regulation of Preautonomic Neuron Activity by Somato-Dendritic Vasopressin Secretion -- Box 4.2 Retrograde Labeling of Axon Projections -- 4.4.3 Autocrine Regulation of Oxytocin Neuron Activity -- 4.4.3.1 Burst Firing in Oxytocin Neurons -- 4.4.3.2 Morphine Dependence in Oxytocin Neurons -- 4.4.3.3 Co-expressed Neuropeptides -- 4.4.4 Paracrine Regulation of Behavior by Somato-Dendritic Oxytocin Secretion -- 4.4.4.1 Regulation of Energy Balance by Somato-Dendritic Oxytocin. , 4.4.4.2 Regulation of Social Behavior by Somato-Dendritic Oxytocin -- 4.5 Perspectives -- Key References: See Main List for Reference Details -- References -- Further Recommended Reading -- 5: Neurosecretory Vesicles: Structure, Distribution, Release and Breakdown -- 5.1 Introduction -- 5.2 Evolution of Neurosecretory Vesicles -- 5.3 Formation of Neurosecretory Vesicles -- 5.4 Dense-Cored and Electron-Lucent Vesicles in Neurosecretory Terminals -- 5.5 Size, Shape and Electron Density of Neurosecretory Dense-Cored Vesicles -- 5.5.1 Preparation Procedure Effects -- 5.5.2 Estimates of Peptide Content of a DCV -- 5.6 Core Content of Neurosecretory Dense-Cored Vesicles -- 5.6.1 Co-packaged Neuroactive Compounds -- 5.6.2 Co-packaged Proteolytic Enzymes and Enzyme Inhibitor -- 5.7 Membrane Proteins of Dense-Cored Vesicles -- 5.7.1 Vesicle Membrane and Core Stability -- 5.8 Dense-Cored Vesicle Trafficking -- 5.9 Are the Vesicles in the Axons and Dendrites Similar? -- 5.10 What Is the Readily Releasable Pool of Dense-Cored Vesicles? -- 5.11 Dense-Cored Vesicles also Transport Receptors to the Cell Surface -- 5.12 Exocytosis of Dense-Cored Neurosecretory Vesicles: Mechanism -- 5.12.1 Location of Exocytosis of Neurosecretory Dense-Cored Vesicles -- 5.13 Destruction of Dense-Cored Vesicles -- 5.14 Conclusions -- Key References: See Main List for Reference Details -- References -- 6: Molecular Controls on Regulated Neurotransmitter and Neurohormone Secretion -- 6.1 Introduction -- 6.2 Calcium-Dependent Exocytosis Is a Multistep Process -- 6.3 Munc-18 -- 6.4 Rab GTPases -- 6.4.1 A Functional Model for Rab3 as a ``Clamp´´ -- 6.4.2 Functional Overlap Between Rab GTPases -- 6.4.3 Regulators of Rab Function -- 6.5 Tomosyn -- Box 6.1 Directly Visualizing Neurotransmitter Release or Vesicle Cycling Using Fluorescence -- 6.5.1 Tomosyn Proteins as ``Clamps´´. , 6.5.2 Proposed Mechanism for Tomosyn Proteins as ``Clamps´´ -- 6.6 Conclusions -- Key References: See Main List for Reference Details -- References -- 7: Secretory Astrocytes -- 7.1 Homoeostatic Astrocytes -- 7.2 Gliocrine System -- 7.3 Mechanisms of Astroglial Secretion -- 7.3.1 Exocytosis and Secretory Organelles in Astrocytes -- 7.3.2 Release Through Plasmalemmal Channels -- 7.3.3 Transporter-Mediated Release -- 7.4 Astroglia-Derived Secretory Molecules -- 7.4.1 Neurotransmitters -- 7.4.2 Neuromodulators -- 7.4.3 Hormones -- 7.4.4 Growth Factors -- 7.4.5 Neuropeptides -- 7.4.6 Polyamines -- 7.5 Astroglial Vesicle Exocytotic Mechanisms -- Box 7.1 Capacitance to Measure Exocytosis -- 7.6 Conclusions and Perspectives -- Key References: See Main List for Reference Details -- References -- 8: Action Potential-Induced Ca2+ Influx for Both Acute and Sustained Insulin Secretion in Pancreatic Beta Cells -- 8.1 Simultaneous Monitoring of Regulatory Molecules and Exocytosis in Pancreatic Beta Cells -- Box 8.1 Patch-Clamp Capacitance Measurement of Exocytosis -- Box 8.2 FRET Imaging -- 8.2 Sustained Insulin Secretion Requires Ca2+-Dependent Vesicle Recycling -- 8.2.1 cAMP/PKA Signaling in Insulin Secretion -- Box 8.3 Simultaneous Recordings of [Ca2+]i and PKA Activity -- 8.2.2 Ca2+-Dependent Adenylyl Cyclase in Pancreatic Beta Cells -- 8.3 Conclusion and Future Directions -- Key References: See Main List for Reference Details -- References -- 9: Plasticity in the Morphology of Lactotrophs and Folliculo-Stellate Cells and Prolactin Secretion -- 9.1 Introduction -- 9.1.1 Lactotrophs, the Prolactin-Secreting Cells of the Anterior Pituitary -- 9.1.2 Prenatal Development of Lactotrophs -- 9.1.3 Postnatal Proliferation of Lactotrophs -- 9.2 Morphological Heterogeneity of Lactotrophs -- 9.2.1 Age and Sex Variation in the Proportion of Lactotroph Subtypes. , 9.2.2 Proportion of Lactotroph Subtypes After Ovariectomy and Estradiol Replacement -- 9.2.3 Estrous Cycle Variation in the Proportion of Lactotroph Subtypes -- 9.2.4 Morphological Subtype Proportions in Pregnancy and Lactation -- 9.2.5 Age-Related Changes in PRL Synthesis, Secretion and Lactotroph Morphology -- 9.3 Functional Heterogeneity of Lactotrophs -- 9.3.1 Different Morphological Types of Lactotroph Respond Differently to PRL Secretagogues -- 9.4 Prolactin Cell Plasticity and Coordination of Prolactin Secretion -- 9.5 Folliculo-Stellate Cells -- 9.5.1 Development of Folliculo-Stellate Cells -- 9.5.2 FS Cell Networks -- 9.5.3 Folliculo-Stellate Cell Function in Paracrine Communication -- 9.5.4 Plasticity in Folliculo-Stellate Cells with Changing Endocrine Status -- 9.5.5 Plasticity of Folliculo-Stellate Cells in Aging -- 9.6 Seasonal Plasticity in Lactotrophs and Folliculo-Stellate Cells in the Ovine Pituitary -- 9.7 Seasonal Plasticity in the Ovine Pituitary Pars Tuberalis -- 9.8 Coordinated Secretion: Relationship Between Pituitary Cells and the Pituitary Vasculature -- 9.9 Conclusions -- Key References: See Main List for Reference Details -- References -- 10: Neuroendocrine and Metabolic Regulation of Plasma Growth Hormone Secretory Profiles -- 10.1 Introduction -- 10.2 Pulsatility: A Fundamental Property of GH Secretion -- 10.2.1 Sex Differences -- 10.2.2 Target Tissue Responses -- 10.2.3 Sleep -- 10.2.4 GH Pattern Summary -- 10.3 Changes of GH Secretion Relative to Energy Balance and Species -- 10.3.1 Adiposity Inversely Correlates to GH Secretion under Positive Energy Balance -- 10.3.1.1 Insulin, a Potent Regulator of GH under Postive Energy Balance -- 10.3.2 GH Secretion in Large Mammals under Negative Energy Balance -- 10.3.3 GH Secretion in Small Mammals under Negative Energy Balance. , 10.3.4 Summary of GH Secretion over Postive or Negative Energy Balance.
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  • 2
    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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  • 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, ...
    Type of Medium: Electronic Resource
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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
    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. ...
    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
    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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  • 9
    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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  • 10
    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.
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