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- W65622118 abstract "Previous electrophysiological experiments have shown that the pyrethroids and DDT cause depolarisation of nerve membranes by prolonging the inward sodium current; in this they resemble the alkaloid veratridine, which is known to interact with the sodium channel in mammalian neurones, causing an influx of sodium ions that results in depolarisation and transmitter release. We report the effect of three insecticides (DDT and two pyrethroids - deltamethrin and permethrin) on transmitter release from guinea-pig synaptosomes. The synaptosomes were maintained in a superfusion system and preloaded with [3H]-γ-Aminobutyric acid ([3H]-GABA). The radioactivity released from the preloaded system comprised [3H]-GABA and a volatile component thought to be tritiated water. All three insecticides caused a concentration-dependent increase in release of [3H]-GABA, with only minor effects on release of tritiated water suggesting that the effect on transmitter release was specific. Deltamethrin was more active than either permethrin or DDT. For deltamethrin, the maximal response was seen at ~10–5M and resulted in a 27% increase in release of radioactivity; the EC50 was ~10–7M and the threshold response lower than 10–8M. Tetrodotoxin (TTX) abolished the effect of deltamethrin and substantially reduced the effect of DDT showing that they interact specifically with the sodium channel. The release of GABA evoked by deltamethrin and DDT was largely independent of the external calcium concentration suggesting that calcium entry into the synaptosome is not a necessary requirement for their action." @default.
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- W65622118 date "1983-01-01" @default.
- W65622118 modified "2023-09-25" @default.
- W65622118 title "PYRETHROID- AND DDT-EVOKED RELEASE OF GABA FROM THE NERVOUS SYSTEM IN VITRO" @default.
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- W65622118 doi "https://doi.org/10.1016/b978-0-08-029224-3.50015-0" @default.
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