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  • 1
    Electronic Resource
    Electronic Resource
    2-Iodomelatonin prevents apoptosis of cerebellar granule neurons via inhibition of A-type transient outward K+ currents (2005)
    Oxford, UK : Munksgaard International Publishers
    Journal of pineal research 38 (2005), S. 0 
    Details
    ISSN: 1600-079X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract:  Compelling evidence indicates that excessive K+ efflux and intracellular K+ depletion are key early steps in apoptosis. Previously, we reported that apoptosis of cerebellar granular neurons induced by incubation under low K+ (5 mm) conditions was associated with an increase in delayed rectifier outward K+ current (IK) amplitude and caspase-3 activity. Moreover, the melatonin receptor antagonist 4P-PDOT abrogated the effects of 2-iodomelatonin on IK augmentation, caspase-3 activity and apoptosis. Here, we show that incubation under low K+/serum-free conditions for 6 hr led to a dramatic increase in the A-type transient outward K+ current (IA) (a 27% increase; n = 31); in addition, fluorescence staining showed that under these conditions, cell viability decreased by 30% compared with the control. Treatment with 2-iodomelatonin inhibited the IA amplitude recorded from control and apoptotic cells in a concentration-dependent manner and modified the IA channel activation kinetics of cells under control conditions. Moreover, 2-iodomelatonin increased the viability of cell undergoing apoptosis. Interestingly, 4P-PDOT did not abrogate the effect of 2-iodomelatonin on IA augmentation under these conditions; in the presence of 4P-PDOT (100 μm), 2-iodomelatonin reduced the average IA by 41 ± 4%, which was similar to the effect of 2-iodomelatonin alone. These results suggest that the neuroprotective effects of 2-idomelatonin are not only because of its antioxidant or receptor-activating properties, but rather that 2-iodomelatonin may inhibit IA channels by acting as a channel blocker.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1600-079X.2004.00174.x
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  • 2
    Electronic Resource
    Electronic Resource
    Adenosine Inhibits L- and N-Type Calcium Channels in Pituitary Melanotrophs. Evidence for the Involvement of a G Protein in Calcium Channel Gating (1996)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neuroendocrinology 8 (1996), S. 0 
    Details
    ISSN: 1365-2826
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: It has been previously demonstrated that activation of A1 adenosine receptors in frog melanotrophs causes inhibition of spontaneous action potential discharges and alpha-melanocyte-stimulating hormone secretion. In the present study, we have investigated the effect of adenosine on high-voltage-activated (HVA) calcium currents in cultured melanotrophs, using the whole-cell variant of the patch-clamp technique with barium as a charge carrier. Adenosine and the specific A1 adenosine receptor agonist R-PIA (50 μM each) produced a decrease of the amplitude of the barium current, while the selective A2 adenosine receptor agonist CGS 21680 did not affect the current. The inhibitory effect of R-PIA was observed throughout the activation range of the current, with stronger responses at more positive potentials. R-PIA inhibited both the L- and N-type components of the current, the effect on the N-component being two-fold higher than on the L-component. The inhibitory effect of R-PIA was rendered irreversible by addition of GTPyS (100 μM) to the intracellular solution. Pre-treatment of the cells with pertussis toxin (1 μg/ml; 12 h) totally abolished the effect of R-PIA on the HVA calcium channels. Conversely, addition of a high concentration of cAMP (100 μM) together with the phosphodiesterase inhibitor IBMX (100 μM) to the intracellular solution did not modify the effect of R-PIA on the current.It is concluded that, in frog melanotrophs, adenosine induces inhibition of L- and N-calcium currents and that this effect is mediated by a pertussis toxin-sensitive G protein. Our data also indicate that the inhibitory effect of adenosine on the calcium currents is not mediated by inhibition of adenylyl cyclase.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2826.1996.tb00827.x
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  • 3
    Electronic Resource
    Electronic Resource
    Melatonin receptor agonist 2-iodomelatonin prevents apoptosis of cerebellar granule neurons via K+ current inhibition (2004)
    Oxford, UK : Munksgaard International Publishers
    Journal of pineal research 36 (2004), S. 0 
    Details
    ISSN: 1600-079X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract:  Activation of K+ current plays a critical role in the control of programmed cell death. In the present study, whole-cell patch-clamp recording, a caspase-3 activity assay, and flow cytometric analysis were used to examine the effects of the MT2 melatonin receptor agonist 2-iodomelatonin on the delayed-rectifier K+ current (IK) and the prevention of apoptosis. It was found that apoptosis of cerebellar granular neurons induced by low-K+ (5 mm) incubation was associated with an increase in IK amplitude and caspase-3 activity. After 6 hr of low-K+ treatment, IK was increased by 45% (n = 86). Flow cytometry showed that the apoptosis rate increased by 333% compared with the control neurons. In addition, exposure of cultured granule cells to low K+ also resulted in a significant activation of caspase-3, by 466%. 2-Iodomelatonin (10 μm in injection pipette) inhibited the IK amplitude recorded from control cells and from cells undergoing apoptosis. However, 2-iodomelatonin only modified the IK-channel activation kinetics of cells under both conditions. Furthermore, 2-iodomelatonin reduced the rate of apoptosis and caspase-3 activation, by 66 and 64%, respectively. The melatonin receptor antagonist, 4P-PDOT, abrogated the effect of 2-iodomelatonin on the IK augmentation, caspase-3 activity, and apoptosis. These results suggest that the neuroprotective effects of melatonin are not only because of its function as a powerful antioxidant, but also to its interactions with specific receptors. The effect of 2-iodomelatonin against apoptosis may be mediated by activating a melatonin receptor, which modulates IK channels and reduces K+ efflux.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1600-079X.2003.00104.x
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    Paper (German National Licenses)
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