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  • 1
    Electronic Resource
    Electronic Resource
    Dual modulation of calcium channel current via recombinant α2-adrenoceptors in pheochromocytoma (PC-12) cells (1997)
    Springer
    Pflügers Archiv 435 (1997), S. 280-285 
    Details
    ISSN: 1432-2013
    Keywords: Key words Calcium channels ; α2-Adrenoceptors ; G proteins ; Dexmedetomidine ; PC-12 cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The ability of recombinant rat α2D-and α2B-adrenoceptors expressed in nerve-growth-factor-differentiated pheochromocytoma PC-12 cells to modulate Ca2+ currents, recorded by the whole-cell patch-clamp technique, has been studied. Ca2+ currents in different cells were either reversibly reduced or increased by dexmedetomidine, an α2-adrenergic agonist, in a concentration-dependent manner. Pertussis toxin pretreatment reduced the number of cells that showed an inhibitory response and reduced the magnitude of inhibition. In cells expressing the α2B-adrenoceptor, pertussis toxin increased the proportion of cells from which a stimulatory effect on Ca2+ currents could be recorded. The magnitude of the inhibitory responses was unaffected but the stimulatory responses were considerably reduced by the dihydropyridine Ca2+ channel blocker nifedipine (5 μM). All effects of dexmedetomidine were reversible upon wash-out and inhibited by the antagonist rauwolscine. The results support the idea that modulation of voltage-dependent Ca2+ channels in transfected PC-12 cells is mediated by activation of recombinant α2D- and α2B-adrenoceptors. This receptor activation predominantly causes inhibition of dihydropyridine-insensitive Ca2+ channels via pertussis-toxin-sensitive G proteins. Additionally receptor activation can also lead to stimulation of dihydropyridine-sensitive Ca2+ channels via pertussis-toxin-insensitive mechanisms.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004240050513
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Endogenous γ-l-glutamylglutamate is a partial agonist at the N-methyl-d-aspartate receptors in cultured cerebellar granule cells (1995)
    Springer
    Neurochemical research 20 (1995), S. 1471-1476 
    Details
    ISSN: 1573-6903
    Keywords: Cerebellar neurons ; N-methyl-d-aspartate receptors ; γ-l-glutamylglutamate ; intracellular Ca2+ depolarization ; Mg2+ dependency
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract γ-l-Glutamylglutamate (LGG), an endogenous constituent of the brain, reduced the glutamateevoked increase in intracellular Ca2+ in cultured cerebellar granule cells. The extent and properties of this inhibition were different at different Mg2+ concentrations. The intracellular Ca2+ response to NMDA was slightly enhanced by 0.1 mM LGG in normal (1.3 mM) Mg2+ medium, but in Mg2+-free medium LGG was stimulatory at low (0.1–1 μM) NMDA and inhibitory at high (0.1–1 mM) NMDA concentrations. In the absence of Mg2+, LGG alone increased cytosolic free Ca2+ and depolarized the cells. These effects were potentiated by glycine and blocked by extracellular Mg2+, 2-amino-5-phosphonopentanoate (APV), 7-chlorokynurenate, 3-amino-1-hydroxypyrrolidin-2-one (HA-966) and 5,7-dinitroquinoxaline-2,3-dione (MNQX). The results indicate that LGG is a partial NMDA agonist. On the other hand, the non-NMDA antagonists 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and 6,7-dinitroquinoxaline-2,3-dione (DNQX) also inhibited the effects of LGG. This indicates an involvement of non-NMDA receptors in the actions of LGG. The consequent depolarization may also contribute to the activation of NMDA receptor-governed ionophores.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00970596
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    Paper (German National Licenses)
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