Effects of dieldrin (HEOD) and some of its metabolites on synaptic transmission in the frog motor end-plate

Akkermans, L.M.A.; Bercken, Joep van den; Zalm, J.M. van der; Straaten, H. W. M. van

doi:10.1016/0048-3575(74)90114-x

Cited by 24 publications

(9 citation statements)

References 33 publications

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“…Time course of the single e.p.p, was not affected by aldrin-transdiol. These results corroborate our earlier observations (Akkermans et al, 1974).…”

Section: End-plate Potentialsupporting

confidence: 94%

“…It should be noted, however, that only an increased influx of calcium during a nerve impulse would lead to increased quantal content coinciding with augmented facilitation, while an accumulation of intracellular calcium as caused by high external calcium (Rahamimoff, 1968) or by cardiac glycosides (Hubbard and Quastel, 1973) would lead to an increase in quantal content without increasing facilitation. On the other hand we have previously demonstrated (Akkermans et al, 1974) that aldrin-transdiol induces a marked increase in spontaneous transmitter release, which is largely independent of the presence of external calcium. This might indicate that aldrin-transdiol could affect a step in the release process in which calcium is probably not essential as does ethanol (Quastel et al, 1971).…”

Section: Discussionmentioning

confidence: 82%

“…In an earlier investigation we demonstrated (Akkermans et al, 1974) that the aldrin-transdiol-induced increase in e.p..p, amplitude in Mg~÷-blocked preparations is of presynaptic origin and is due to an increase in quantal content. In the present study a significant increase in e.p.p, size was also observed in junctions where the process of transmitter release is not impaired, i.e., in curarized junctions.…”

Section: Discussionmentioning

confidence: 93%

“…In this case, however, the increase in e.p.p, amplitude is much smaller than under conditions of low quantal content, and even absent at times. Since aldrin-transdiol has a postsynaptic blocking action as well (Akkermans et al, 1974) this might indicate that aldrin-transdiol and d-tubocurarine have a synergistic action on the postsynaptic membrane. However, no clear correlation could be established between the concentration of dtubocurarine and the effect of aldrin-transdiol on e.p.p, amplitude.…”

Section: Discussionmentioning

confidence: 99%

“…However, no clear correlation could be established between the concentration of dtubocurarine and the effect of aldrin-transdiol on e.p.p, amplitude. On the other hand it could be that at higher values of quantal content aldrin-transdiol causes earlier exhaustion of transmitter stores in the terminals; the more because aldrin-transdiol also increases spontaneous release (Akkermans et al, 1974).…”

Section: Discussionmentioning

confidence: 99%

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Effects of Aldrin-transdiol on neuromuscular facilitation and depression

Akkermans

Bercken

Zalm

1975

European Journal of Pharmacology

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Effects of aldrin-transdiol on neuromuscular facilitation and depression, European J. Pharmacol. 31 (1975) 166--175.The effects of aldrin-transdiol, one of the active metabolites of the insecticide dieldrin, on evoked transmitter release, neuromuscular facilitation and neuromuscular depression have been studied in frog sartorius nerve--muscle preparations. Conventional techniques of intracellular recordings were used. Aldrin-transdiol caused a marked increase in end-plate potential amplitude under conditions of low quantal content, i.e., in Mg2+-blocked junctions. The increase in end-plate potential amplitude was less pronounced in curarized junctions, in which the transmitter release was not impaired. Concomitant with the increase in end-plate potential size there was a marked enhancement of facilitation during short trains of stimuli applied to the motor nerve. The decay of facilitation was, however, not seriously affected by aldrin-transdiol. These effects may be explained in terms of the known 'calcium hypothesis' by assuming that aldrin-transdiol increases the amount of calcium which enters the nerve terminal during the nerve impulse.The increase in end-plate potential amplitude and in facilitation by aldrin-transdiol was transient. At later stages of poisoning, end-plate potential and facilitation decreased below control level and neuromuscular depression was significantly enhanced. This latter effect may be the result of a direct inhibitory effect of aldrin-transdiol on transmitter mobilization. As far as the fall in end-plate potential amplitude is concerned the known suppressive action of aldrin-transdiol on the chemical sensitivity of the postsynaptic membrane and on the nerve action potential probably plays a part as well. Finally, neuromuscular transmission was completely blocked by aldrintransdiol.

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“…Time course of the single e.p.p, was not affected by aldrin-transdiol. These results corroborate our earlier observations (Akkermans et al, 1974).…”

Section: End-plate Potentialsupporting

confidence: 94%

Section: Discussionmentioning

confidence: 82%

Section: Discussionmentioning

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Effects of Aldrin-transdiol on neuromuscular facilitation and depression

Akkermans

Bercken

Zalm

1975

European Journal of Pharmacology

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Phenylpyrazoles, a new class of pesticide: Effects on neuromuscular transmission and acetylcholine responses

et al. 1991

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Phenylpyrazoles constitute a newly developed class of chemicals with insecticidal and herbicidal properties. In acute toxicity experiments in rats, near‐lethal doses of phenylpyrazoles produce neurotoxic symptoms with an unknown mode of action. We have investigated the effects of two phenylpyrazoles, SLA4722 and SLA4685, in the frog neuromuscular junction and in the clonal muscle cell line BC3H‐1. In the frog neuromuscular junction SLA4722 at concentrations ⩾ 10−5 M caused a pronounced increase in the frequency of miniature endplate potentials (MEPPs). SLA4685 caused a similar increase but was less potent. In the clonal muscle cell line BC3H‐1, SLA4685 produced a concentration‐dependent block of the acetylcholine (ACh) response (IC50 = 2.4(±0.3) × 10−5 M). At 10−6 M a slight potentiating effect of SLA4685 on the ACh response was observed. SLA4722 was less potent in this preparation. The increased transmitter release might, at least partly, be responsible for the excitatory effects of the phenylpyrazoles in intact animals.

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