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  • 1
    Electronic Resource
    Electronic Resource
    Activation and Inactivation of Oxytocin and Vasopressin Release from Isolated Nerve Endings (Neurosecretosomes) of the Rat Neurohypophysis (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: Neurosecretory terminals (neurosecretosomes, NSS) were isolated from rat neurohypophyses. High [K+]oor veratridine stimulated secretion of vasopressin and oxytocin by up to ∼ 100-fold. Stimulated secretion was dependent on calcium and temperature, and could be elicited from NSS maintained in culture for 4 days. After overnight culture of the NSS, secretion was still inhibited by calcium channel blockers (cobalt, dihydropyridines, ω-conotoxin, D 600) and K opiates (dynorphin and U50488). Ionomycin evoked dose and calcium-dependent hormone release, with a Hill coefficient for calcium of 1.74. High [K+]o enhanced the 5 μMionomycin-induced secretion, apparently through calcium entry rather than depolarization, as the increase in secretion was abolished by 100 μM D 600. During prolonged depolarization the hormone secretion peaked within 2 min, then declined to near basal levels. Depolarization for 25 min without calcium neither activated secretion nor prevented subsequent secretion on readdition of calcium, suggesting that the decline in secretion was not due to membrane depolarization. Indeed, the rates of decline in secretion were similar for different levels of depolarization (0.070 ± 0.003 and 0.081 ± 0.003 min−1 for 25 and 45 mM [K+]o, respectively). Four minutes after the onset of continuous depolarization (45 mM[K+]o) in the presence of calcium, the declining secretion was still dependent on voltage-activated calcium influx through channels sensitive to D 600 and nitrendipine. The results presented here suggest that the decline in secretion during prolonged depolarizing stimuli may be due to exhaustion, inactivation, or desensitization of a calcium-triggered event.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1991.tb03779.x
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  • 2
    Electronic Resource
    Electronic Resource
    Characterization of K Opioid Receptors in Neurosecretosomes from Bovine Posterior Pituitary (1987)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 49 (1987), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The binding properties of opioid receptors on isolated nerve terminals (neurosecretosomes) from bovine posterior pituitaries were characterized. Both [3H]etorphine and [3H]ethylketocyclazocine ([3H]EKC) showed high-affinity binding with complex binding isotherms, consistent with the presence of multiple classes of binding sites. [D-Ala2,D-Leu5]enkephalin showed no specific binding and failed to displace [3H]etorphine at high concentrations, indicating the absence of μ, δ, or benzomorphan (K2) sites. Mathematical modelling of the data suggested the presence of three classes of binding sites. The first was of high affinity with Kd values of 0.9 and 2.0 nM for etorphine and EKC, respectively. The second class of sites appeared to bindetorphine with a KD of 150 nM, and EKC with extremely low affinity (unmeasurable binding). The third class of sites was characterized by KD values of 7 and 2 μM for etorphine and EKC, respectively. These results indicate that the nerve terminals of bovine posterior pituitary contain opioid binding sites of the K type. Futhermore, these binding sites appear heterogeneous, consisting of at least two and possibly more subtypes or states.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1987.tb02882.x
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  • 3
    Electronic Resource
    Electronic Resource
    Effect of Tetanus Toxin on Oxytocin and Vasopressin Release from Nerve Endings of the Neurohypophysis (1990)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 55 (1990), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The effect of tetanus toxin on neuropeptide hormone release from isolated nerve endings of the neural lobe of rat pituitaries (neurosecretosomes) was measured in a perfusion system. Tetanus toxin inhibited depolarization-evoked release of oxytocin and vasopressin in a time- and dose-dependent manner. At 1 μg/ml, tetanus toxin blocked stimulated release by 85%. Tetanus toxin that was preincubated with a neutralizing monoclonal antibody or heated to 100°C had no effect on hormone release. The ionophores A23187 and ionomycin were potent stimulators of hormone release in control nerve endings, but were not able to overcome the effect of tetanus toxin in intoxicated nerve endings. 8-Bromo cyclic GMP. which has been reported to reverse the action of tetanus toxin in PC12 cells, had no effect on the action of tetanus toxin in neurosecretosomes. Neurosecretosomes are the first system in which tetanus toxin has been shown to block release from peptidergic nerve terminals. They appear to be a valuable in vitro system for studying the biochemical mechanism of tetanus toxin action.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1990.tb05797.x
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  • 4
    Electronic Resource
    Electronic Resource
    Comparison of Type 2 Inositol 1,4,5-Trisphosphate Receptor Distribution and Subcellular Ca2+ Release Sites that Support Ca2+ Waves in Cultured Astrocytes (1997)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 68 (1997), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: We have examined the mechanisms that underlie Ca2+ wave propagation in cultured cortical astrocytes. Norepinephrine evoked Ca2+ waves in astrocytes that began at discrete initiation loci and propagated throughout the cell by regenerative amplification at a number of cellular sites, as shown by very high Ca2+ release rates at these regions. We have hypothesized previously that domains displaying elevated Ca2+ release kinetics in astrocytes may correspond to sites of high inositol 1,4,5-trisphosphate receptor (InsP3R) density. To examine this possibility, we compared the distribution pattern of endoplasmic reticulum (ER) and InsP3Rs with Ca2+ release kinetics in subcellular regions during propagation of norepinephrine-evoked waves. 3,3′-Dihexyloxacarbocyanine iodide staining revealed that the ER in astrocytes exists as a meshwork of membranes extending throughout the cells, including fine processes. A specific antibody directed against type 2 InsP3Rs (InsP3R2) detected a 260-kDa band in western blotting of astrocyte membranes. Immunocytochemistry using this antibody stained the entire ER system in a punctate, variegated manner. When Ca2+ responses and InsP3R2 immunofluorescence were compared in the same cell, domains of elevated Ca2+ response kinetics (high amplitude and rapid rate of rise) showed significant positive correlation with high local intensity of InsP3R2 staining. It appears, therefore, that specializations in the ER responsible for discrete local Ca2+ release sites that support regenerative wave propagation include increased levels of InsP3R2 expression.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1997.68062317.x
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  • 5
    Electronic Resource
    Electronic Resource
    Mitochondria regulate Ca2+ wave initiation and inositol trisphosphate signal transduction in oligodendrocyte progenitors (2002)
    Oxford, UK : Blackwell Science, Ltd
    Journal of neurochemistry 80 (2002), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Mitochondria in oligodendrocyte progenitor cells (OPs) take up and release cytosolic Ca2+ during agonist-evoked Ca2+ waves, but it is not clear whether or how they regulate Ca2+ signaling in OPs. We asked whether mitochondria play an active role during agonist-evoked Ca2+ release from intracellular stores. Ca2+ puffs, wave initiation, and wave propagation were measured in fluo-4 loaded OP processes using linescan confocal microscopy. Mitochondrial depolarization, measured by tetramethyl rhodamine ethyl ester (TMRE) fluorescence, accompanied Ca2+ puffs and waves. In addition, waves initiated only where mitochondria were localized. To determine whether energized mitochondria were necessary for wave generation, we blocked mitochondrial function with the electron transport chain inhibitor antimycin A (AA) in combination with oligomycin. AA decreased wave speed and puff probability. These effects were not due to global changes in ATP. We found that AA increased cytosolic Ca2+, markedly reduced agonist-evoked inositol trisphosphate (IP3) production, and also enhanced phosphatidylinositol 4,5-bisphosphate (PIP2) binding to the Ca2+ dependent protein gelsolin. Thus, the reduction in puff probability and wave speed after AA treatment may be explained by competition for PIP2 between phospholipase C and gelsolin. Energized mitochondria and low cytosolic Ca2+ concentration may be required to maintain PIP2, a substrate for IP3 signal transduction.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.0022-3042.2001.00727.x
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  • 6
    Electronic Resource
    Electronic Resource
    Presynaptic Modulation of Oxytocin and Vasopressin Secretion from Isolated Nerve Terminals of the Rat Neural Lobe (1990)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 604 (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.tb32047.x
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  • 7
    Electronic Resource
    Electronic Resource
    Subcellular calcium oscillators and calcium influx support agonist-induced calcium waves in cultured astrocytes (1995)
    Springer
    Molecular and cellular biochemistry 149-150 (1995), S. 137-144 
    Details
    ISSN: 1573-4919
    Keywords: calcium oscillations ; astrocytes ; calcium influx
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract We have analysed Ca2+ waves induced by norepinephrine in rat cortical astrocytes in primary culture using fluorescent indicators fura-2 or fluo-3. The temporal pattern of the average [Ca2+]i responses were heterogeneous from cell to cell and most cells showed an oscillatory response at concentrations of agonist around EC50 (200 nM). Upon receptor activation, [Ca2+]i signals originated from a single cellular locus and propagated throughout the cell as a wave. Wave propagation was supported by specialized regenerative calcium release loci along the length of the cell. The periods of oscillations, amplitudes, and the rates of [Ca2+]i rise of these subcellular oscillators differ from each other. These intrinsic kinetic properties of the regenerative loci support local waves when stimulation is continued over long periods of time. The presence of local waves at specific, invariant cellular sites and their inherent kinetic properties provide for the unique and reproducible pattern of response seen in a given cell. We hypothesize that these loci are local specializations in the endoplasmic reticulum where the magnitude of the regenerative Ca2+ release is higher than other regions of the cell. Removal of extracellular Ca2+ or blockade of Ca2+ channels by inorganic cations (Cd2+ and Ni2+) during stimulation of adrenergic receptors alter the sustained plateau component of the [Ca2+]i response. In the absence of Ca2+ release, due to store depletion with thapsigargin, agonist occupation alone does not induce Ca2+ influx in astrocytes. This finding suggests that, under these conditions, receptor-operated Ca2+ entry is not operative. Furthermore, our experiments provide evidence for local Ca2+ oscillations in cells which can support both wave propagation as well as spatially discrete Ca2+ signalling.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01076572
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  • 8
    Electronic Resource
    Electronic Resource
    Mitochondria in Ca2+ Signaling and Apoptosis (2000)
    Springer
    Journal of bioenergetics and biomembranes 32 (2000), S. 35-46 
    Details
    ISSN: 1573-6881
    Keywords: Ca2+ signaling ; inositol 1,4,5-trisphosphate receptor ; mitochondrial Ca2+ uptake ; mitochondrial Ca2+ efflux ; permeability transition ; apoptosis ; Bcl-2 family
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Physics
    Notes: Abstract Cellular Ca2+ signals are crucial in the control of most physiological processes, cell injuryand programmed cell death; mitochondria play a pivotal role in the regulation of such cytosolicCa2+ ([Ca2+]c) signals. Mitochondria are endowed with multiple Ca2+ transport mechanismsby which they take up and release Ca2+ across their inner membrane. These transport processesfunction to regulate local and global [Ca2+]c, thereby regulating a number of Ca2+-sensitivecellular mechanisms. The permeability transition pore (PTP) forms the major Ca2+ effluxpathway from mitochondria. In addition, Ca2+ efflux from the mitochondrial matrix occursby the reversal of the uniporter and through the inner membrane Na+/Ca2+ exchanger. Duringcellular Ca2+ overload, mitochondria take up [Ca2+]c, which, in turn, induces opening of PTP,disruption of mitochondrial membrane potential (ΔΨm) and cell death. In apoptosis signaling,collapse of ΔΨ;m and cytochrome c release from mitochondria occur followed by activationof caspases, DNA fragmentation, and cell death. Translocation of Bax, an apoptotic signalingprotein from the cytosol to the mitochondrial membrane, is another step during thisapoptosis-signaling pathway. The role of permeability transition in the context of cell death in relationto Bcl-2 family of proteins is discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1005508311495
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  • 9
    Electronic Resource
    Electronic Resource
    Sodium inhibits hormone release and stimulates calcium efflux from isolated nerve endings of the rat neurohypophysis (1991)
    Springer
    Cellular and molecular neurobiology 11 (1991), S. 321-331 
    Details
    ISSN: 1573-6830
    Keywords: secretion ; oxytocin ; vasopressin ; neurosecretosomes ; ionomycin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary 1. We studied the effects of extracellular sodium on the secretion of vasopressin (VP) and oxytocin (OT) and the efflux of45Ca from isolated, perfused nerve endings of the rat neurohypophysis (neurosecretosomes). 2. Upon removal of sodium from the perfusing medium, basal release of VP and OT increased by 3.95 ± 0.23- and 3.71 ± 0.22-fold, respectively, followed by a decline to about double the levels in normal (150 mM) sodium (P ⩽ 0.1). 3. Compared to neurosecretosomes perfused in normal (150 mM) sodium, omission of sodium from the medium augmented ionomycin-induced VP and OT secretion by 66 ± 5- and 20 ± 3-fold, respectively, and A23187-induced secretion was increased 1.3 ± 0.4- and 1.3 ± 0.1-fold (P ⩽ 0.01 for both ionophores). 4. The inhibition of ionomycin-induced secretion by sodium was concentration dependent (P ⩽ 0.01 for sodium ⩾ 5 mM); the IC50 was about 10 mM sodium for both hormones, and the Hill slope was close to -1. 5. The rate of45Ca efflux from neurosecretosomes showed 2.7 ± 0.1-fold stimulation upon increasing sodium from 4.5 to 150 mM (P ⩽ 0.01). 6. Our results suggest that sodium inhibits basal and stimulated secretion at the nerve terminal, possibly by reducing intraterminal calcium through sodium/calcium exchange.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00713276
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  • 10
    Electronic Resource
    Electronic Resource
    Phylogenetic cross-reactivities of monoclonal antibodies produced against rat neurophysin (1984)
    Springer
    Cellular and molecular neurobiology 4 (1984), S. 339-349 
    Details
    ISSN: 1573-6830
    Keywords: monoclonal antibodies ; neurophysin ; phylogenetic ; antibody crossreactivity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary 1. Previously described mouse monoclonal antibodies against rat neurophysins [Ben-Barak, Y.,et al. (1985); Whitnall, M. H.,et al. (1985)] were studied here for their crossreactivities to neurophysins (NPs) from other vertebrate species. 2. Posterior pituitary extracts from various mammals (rat, mouse, cow, human) and lower vertebrates (frog, ratfish) were studied. 3. The monoclonal antibodies displayed several distinct patterns of crossreactivity to the various species, indicating that the epitopes which they recognized were different. PS 67 bound strongly to rat pituitary extract in solid-phase radioimmunoassay (RIA) but showed no cross-reactivity with extracts from any of the other species tested, including the mouse. PS 36 cross-reacted with mouse and frog extracts but showed almost no cross-reactivity with cow and none to ratfish extracts. PS 41 cross-reacted with mouse, cow, and frog extracts. PS 45 was the most cross-reactive antibody and recognized an antigen in extracts from mouse, cow, frog, and ratfish pituitaries. 4. Electrophoresis of proteins extracted from posterior pituitaries, followed by immunoblot staining with either PS 36 or PS 45, demonstrated that the NP-like molecules within each species are heterogeneous, i.e., more than two bands stained in each species. The frog NP stained by PS 45 was about twice the molecular weight of the mammalian NPs. 5. The possible valve of the PS 45 antibody for future molecular cloning experiments on the arginine vasotocin precursor in lower vertebrates is discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00733596
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