Evidence for a presynaptic action of chlordimeform at the insect neuromuscular junction

Yamamoto, Daisuke; Washio, Hiroshi; Fukami, Jun-ichi

doi:10.1002/arch.940010105

Cited by 5 publications

(1 citation statement)

References 28 publications

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“…The present experiments showed unequivocally that dipicolinic acid blocked the neuromuscular transmission by inhibiting the evoked transmitter release from the presynaptic axon terminal with no effect on the postsynaptic membrane. A similar inhibition of evoked release of transmitter has been reported at the mealworm junction treated with a formamidine pesticide chlordimeform [12]. Chlordimeform had little or no effect on spontaneous transmitter release, however.…”

Section: Discussionsupporting

confidence: 77%

The mechanism of block of glutamate synapses by dipicolinic acid

Yamamoto¹,

Miyamoto²,

Oda³

et al. 1985

Arch Insect Biochem Physiol

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The effect of dipicolinic acid (2,6-pyridine dicarboxylic acid) on the mealworm neurornuscular junction was studied using conventional microelectrode recording techniques. Dipicolinic acid (10-5-10-3 M) added to the bathing solution reversibly blocked neuromuscular transmission. The depolarization in response to iontophoretically applied L-glutamate (glutamate potential) was not affected by dipicolinic acid even when the neurally evoked excitatory postsynaptic potential (EPSP) was totally abolished. Focal extracellular recordings from single synaptic sites revealed that in the presence of 1 x M dipicolinic acid the presynaptic spike was unchanged, but the quanta1 content for evoked transmitter release was reduced. The calcium-dependent action potential elicited by direct stimulation of the muscle fiber was not impaired by dipicolinic acid. These results suggest that dipicolinic acid interferes with the transmitter-releasing mechanism from the presynaptic terminal.

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Section: Discussionsupporting

confidence: 77%

The mechanism of block of glutamate synapses by dipicolinic acid

Yamamoto¹,

Miyamoto²,

Oda³

et al. 1985

Arch Insect Biochem Physiol

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The actions of formamidine pesticides on identified central neurones of Helix aspersa

1985

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Membrane potential and voltage clamp measurements of the responses to octopamine, dopamine, 0-acetylcholine, and the formamidine derivatives chlordimeform (CDM) and N'-demethylchlordimeform (DCDM) have bee3 made on identified central neurones of Helix aspersa. DCDM and CDM were agonists on both the inhibitory and excitatory octopamine receptors on these neurones but were less potent than octopamine. The direct inhibitory effect of DCDM was antagonised by both phentolamine and cyproheptadine. DCDM was also found to antagonise the effects of octopamine, dopamine and 0-acetylcholine on these neurones. The pA2 values for DCDM against dopamine and 0-acetylcholine were 5.2 (kO.l) and 5.35 (+0.15), respectively. The pA2 value=log[DR-(UZ)], where 1 is the concentration of the antagonist, and DR=dose ratio =A2/Al; A1 is the dose of agonist required to produce 50% of the maximum response, and A2 is the dose of agonist needed to produce the same degree of response in the presence of the antagonist. It is concluded that DCDM and CDM act specifically on the octopamine receptors of H . aspersa central neurones, both as agonists and antagonists. The antagonist effect of DCDM against dopamine receptors is probably non-specific.

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The Action of Glutamate Agonists at Insect Neuromuscular Junction

Fukami¹

1986

Membrane Receptors and Enzymes as Targets of Insecticidal Action

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Evidence for a presynaptic action of chlordimeform at the insect neuromuscular junction

Cited by 5 publications

References 28 publications

The mechanism of block of glutamate synapses by dipicolinic acid

The mechanism of block of glutamate synapses by dipicolinic acid

The actions of formamidine pesticides on identified central neurones of Helix aspersa

The Action of Glutamate Agonists at Insect Neuromuscular Junction

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