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• W2022347049 abstract "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 m m ) conditions was associated with an increase in delayed rectifier outward K + current ( I K ) amplitude and caspase‐3 activity. Moreover, the melatonin receptor antagonist 4P‐PDOT abrogated the effects of 2‐iodomelatonin on I K 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 ( I A ) (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 I A amplitude recorded from control and apoptotic cells in a concentration‐dependent manner and modified the I A 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 I A augmentation under these conditions; in the presence of 4P‐PDOT (100 μ m ), 2‐iodomelatonin reduced the average I A 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 I A channels by acting as a channel blocker." @default.
• W2022347049 created "2016-06-24" @default.
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• W2022347049 date "2004-09-28" @default.
• W2022347049 modified "2023-10-11" @default.
• W2022347049 title "2-Iodomelatonin prevents apoptosis of cerebellar granule neurons via inhibition of A-type transient outward K+ currents" @default.
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• W2022347049 doi "https://doi.org/10.1111/j.1600-079x.2004.00174.x" @default.
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