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Endplate channel block by guanidine derivatives

J M Farley, J Z Yeh, S Watanabe

The Journal of General Physiology

|March 1, 1981

Summary

n-alkyl guanidines affect frog neuromuscular junctions. Some stimulate transmitter release, while all block acetylcholine receptors, with octylguanidine being most potent.

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Area of Science:

Neuroscience
Pharmacology
Electrophysiology

Background:

The neuromuscular junction (NMJ) is crucial for muscle contraction.
Guanidine derivatives are known to modulate neuronal function.

Purpose of the Study:

To investigate the presynaptic and postsynaptic effects of n-alkyl guanidine derivatives on the frog NMJ.
To elucidate the mechanism of action of these compounds on neurotransmission.

Main Methods:

Two-microelectrode voltage clamp technique.
Electrophysiological recordings of nerve-evoked responses.
Application of n-alkyl guanidines and acetylcholine.

Main Results:

Methyl-, ethyl-, and propylguanidine enhanced nerve-evoked transmitter release.
All derivatives inhibited postsynaptic acetylcholine responses, with octylguanidine being the most potent.
Compounds likely block the ion channel rather than binding to the acetylcholine receptor.
Differential effects on inward and outward endplate currents observed, indicating channel modulation.

Conclusions:

n-Alkyl guanidines exhibit dual effects at the frog NMJ: presynaptic facilitation and postsynaptic blockade.
The mechanism involves ion channel interaction, not direct receptor binding.
Octylguanidine shows potent open and closed channel block kinetics.

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