Key result
Deltamethrin prolonged sodium currents in mouse neuroblastoma cells by several orders of magnitude, stabilizing a variety of channel states by reducing the transition rates between them.
Deltamethrin stabilizes various sodium channel states in mouse neuroblastoma cells, reducing transition rates between them.
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May inform pyrethroid toxicity mechanisms; leaves open translation to human cardiac sodium channel effects.
The effect of the pyrethroid insecticide deltamethrin on sodium channels of mouse neuroblastoma cells was investigated using the patch-clamp technique. The study was aimed at determining how the effects of deltamethrin at the whole cell level would be reflected in the modified properties of single sodium channel currents. Whole cell recording showed that deltamethrin prolonged sodium currents in neuroblastoma cells by several orders of magnitude. Single channel recordings showed that a variety of channel states were prolonged by deltamethrin. Not only was the open state prolonged by several orders of magnitude but a closed or inactivated state was also prolonged, leading to less frequent channel openings. A subconducting state and a flickering state were observed in the presence of deltamethrin as well as a state in which channels opened with some delay after the termination of a depolarizing pulse. The results are compatible with the hypothesis that deltamethrin stabilizes a variety of channel states by reducing the transition rates between them. This allows states that are normally very brief to be detected more easily.
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Chinn et al. (1986) studied this question. Deltamethrin was evaluated on Sodium channel states and currents. Deltamethrin prolonged sodium currents in mouse neuroblastoma cells by several orders of magnitude, stabilizing a variety of channel states by reducing the transition rates between them.
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