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  • 1
    Electronic Resource
    Electronic Resource
    Involvement of Calcineurin in Ca2+ Paradox-Like Injury of Cultured Rat Astrocytes (1998)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 70 (1998), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The Ca2+/calmodulin-dependent phosphatase calcineurin may have physiological and pathological roles in neurons, but little is known about the roles of the enzyme in glial cells. We have previously reported that reperfusion of cultured astrocytes in Ca2+-containing medium after exposure to Ca2+-free medium caused Ca2+ influx followed by delayed cell death. In this study, we examined if calcineurin is involved in this Ca2+-mediated astrocytic injury. FK506, an inhibitor of calcineurin, protected cultured rat astrocytes against paradoxical Ca2+ challenge-induced injury in a dose-dependent manner (10−10–10−8M). Cyclosporin A at 1 µM mimicked the effect of FK506. Rapamycin (1 µM) did not affect astrocyte injury, but it blocked the protective effect of FK506. Deltamethrin (20 nM), another calcineurin inhibitor, had a similar protective effect, whereas okadaic acid did not. FK506 affected neither paradoxical Ca2+ challenge-induced increase in cytosolic Ca2+ level nor Na+-Ca2+ exchange activity in the cells, suggesting that the calcineurin is involved in processes downstream of increased cytosolic Ca2+ level. Immunochemical studies showed that both calcineurin A (probably the Aβ2 isoform) and B subunits were expressed in the cells. It is concluded that calcineurin is present in cultured astrocytes and it has a pathological role in the cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1998.70052004.x
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  • 2
    Electronic Resource
    Electronic Resource
    Intracerebroventricular treatment of mice with pertussis toxin induces hyperalgesia and enhances 3H-nitrendipine binding to synaptic membranes: Similarity with morphine tolerance (1990)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 341 (1990), S. 123-127 
    Details
    ISSN: 1432-1912
    Keywords: GTP-binding protein ; Pertussis toxin ; Morphine tolerance ; 3H-Nitrendipine binding
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of intracerebroventricular treatment of mice with pertussis toxin (PTX) on pain perception and 3H-nitrendipine binding was examined to study a possible change in the GTP-binding proteins in morphine tolerant rodents. It was observed that both PTX treatment and chronic administration of morphine cause hyperalgesia in the acetic acid-induced writhing test. Analgesic effects brought by the acute administration of morphine or nifedipine, a calcium antagonist, were not affected by PTX treatment. In synaptic membrane fractions prepared from mice treated with PTX or morphine chronically, specific binding of 3H-nitrendipine was enhanced approximately 41.8% and 35.7%, respectively, without alteration in its affinity. Chronic administration of morphine followed by PTX treatment did not display further increases in 3H-nitrendipine binding. These results suggest that the PTX-sensitive GTP-binding proteins may not be involved in the manifestation of the analgesic effect of morphine in mice.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00195068
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  • 3
    Electronic Resource
    Electronic Resource
    Potentiation of Carbachol-Induced Ca2+ Release by Peroxynitrite in Human Neuroblastoma SH-SY5Y Cells (2000)
    Springer
    Neurochemical research 25 (2000), S. 909-914 
    Details
    ISSN: 1573-6903
    Keywords: Nitric oxide ; nitration ; phosphorylation ; calcium signaling ; neuroblastoma
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We have investigated the effect of 3-morpholinosydnonimine (SIN-1), a peroxynitrite donor, on carbachol-induced increase in intracellular Ca2+ concentration ([Ca2+]i) in human neuroblastoma SH-SY5Y cells by means of single cell imaging of [Ca2+]i. SIN-1 potentiated carbachol-induced [Ca2+]i rise regardless of external Ca2+, and the potentiation was completely inhibited by superoxide dismutase, indicating that peroxynitrite may enhance Ca2+ release from intracellular stores. On the other hand, SIN-1 reduced carbachol-induced inositol 1,4,5-trisphosphate (IP3) formation. Genistein, a tyrosine kinase inhibitor, potentiated carbachol-induced rise of [Ca2+]i regardless of external Ca2+. These results suggest that peroxynitrite may potentiate the release of Ca2+ from intracellular stores through the perturbation of regulation in tyrosine phosphorylation-dephosphorylation system.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1007540005737
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  • 4
    Electronic Resource
    Electronic Resource
    Cytochalasin B inhibits phosphoinositide hydrolysis in rat hippocampal slices (1993)
    Springer
    Neurochemical research 18 (1993), S. 225-229 
    Details
    ISSN: 1573-6903
    Keywords: Cytochalasin B ; phosphoinositide hydrolysis ; cytoskeleton ; neuronal cell ; hippocampus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effect of cytochalasin B on phosphoinositide (PI) hydrolysis was examined in rat hippocampal slices. Pretreatment of the slices with cytochalasin B caused a significant decrease in PI hydrolysis elicited by carbachol, norepinephrine, or by high K+. This effect was cytochalasin B dose- and time-dependent and was not mimicked by cytochalasin D, vinblastine, colchicine, or phloretin. In contrast, in [3H]inositol-prelabeled hippocampal membranes, cytochalasin B did not affect PI hydrolysis elicited by GTPγS and GTPγS plus carbachol. Similar result was obtained using the membranes prepared from the slices pretreated with cytochalasin B. The inhibitory effect of cytochalasin B on the carbachol-response was observed in SK-N-SH human neuroblastoma cells, but not in cultured rat astrocytes. These results indicate that cytochalasin B inhibits PI hydrolysis in neuron-specific manner and that its action may be an indirect cellular mechanism other than interaction with cytoskeleton elements.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01474688
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  • 5
    Electronic Resource
    Electronic Resource
    The Na+-Ca2+ Exchange Inhibitor KB-R7943 Inhibits High K+-Induced Increases in Intracellular Ca2+ Concentration and [3H]Noradrenaline Release in the Human Neuroblastoma SH-SY5Y (2000)
    Springer
    Neurochemical research 25 (2000), S. 385-387 
    Details
    ISSN: 1573-6903
    Keywords: Na+-Ca2+ exchange ; KB-R7943 ; inhibitor ; noradrenaline release
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of the Na+-Ca2+ exchange inhibitor 2-[2-[4-(4-nitrobenzyloxy)phenyl]ethyl]isothiourea methanesulfonate (KB-R7943) on depolarization-induced Ca2+ signal and [3H]noradrenaline release were examined in SH-SY5Y cells. KB-R7943 at 10 μM significantly inhibited high K+-induced increase in intracellular Ca2+ concentration. KB-R7943 also inhibited high K+-evoked release of [3H]noradrenaline from the cells. These findings suggest that the Na+-Ca2+ exchanger in the reverse mode is involved at least partly in depolarization-induced transmitter release.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1007597105714
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  • 6
    Electronic Resource
    Electronic Resource
    Structure and Function of G Protein Coupled Receptors (1990)
    Springer
    Pharmaceutical research 7 (1990), S. 1213-1221 
    Details
    ISSN: 1573-904X
    Keywords: G protein coupled receptors ; neurotransmitter receptors ; hormone receptors ; adrenergic receptors ; muscarinic cholinergic receptors ; second messengers
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Abstract The G protein coupled receptors (GPC-Rs) comprise a large superfamily of genes encoding numerous receptors which all show common structural features, e.g., seven putative membrane spanning domains. Their biological functions are extremely diverse, ranging from vision and olfaction to neuronal and endocrine signaling. The GPC-Rs couple via multiple G proteins to a growing number of recognized second messenger pathway, e.g., cAMP and phosphatidyl inositol turnover. This review summarizes our current knowledge of the molecular mechanisms by which the GPC-Rs activate second messenger systems, and it addresses their regulation and structure.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1015969301407
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