An electrophysiological study of the action of methylmercuric chloride and mercuric chloride on the sciatic nerve-sartorius muscle preparation of the frog.

doi:10.1016/0041-008X(76)90097-1

Paper

An electrophysiological study of the action of methylmercuric chloride and mercuric chloride on the sciatic nerve-sartorius muscle preparation of the frog.

Published Aug 1, 1976 · Ming Shing Juang

Toxicology and applied pharmacology

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66

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Abstract

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In Vitro Study

Study Snapshot

Methylmercuric chloride primarily affects presynaptic sites, while mercuric chloride affects both pre- and postsynaptic sites in the frog sciatic nerve-sartorius muscle preparation.

PopulationOlder adults (50-71 years)

Sample size24

MethodsObservational

OutcomesBody Mass Index projections

ResultsSocial networks mitigate obesity in older groups.

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Paper

An electrophysiological study of the action of methylmercuric chloride and mercuric chloride on the sciatic nerve-sartorius muscle preparation of the frog.

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References

Evoked transmitter release increased by inorganic mercury at frog neuromuscular junction

Low concentrations of mercury ions (1 M or less) increase the amount of transmitter released from motor nerve terminals, potentially due to mercury ions forming disulphide bridges with sulphydryl groups.

Increased spontaneous transmitter release from presynaptic nerve terminal by methylmercuric chloride

Methylmercury chloride increases spontaneous transmitter release from presynaptic nerve terminals in the sympathetic ganglia, potentially targeting this pathway in the early stages of mercury poisoning.

Antagonism of Neuromuscular Blocks by Germine Monoacetate

Germine monoacetate (GMA) antagonizes neuromuscular blockades, allowing faster evoked action potentials in direct shock-treated muscles, without affecting endplate potential amplitude.

Effect of manganese and lanthanum on spontaneous release of acetylcholine at frog motor nerve terminals.

Manganese and lanthanum enhance spontaneous release of acetylcholine at frog motor nerve terminals, suggesting that they may play a role in regulating acetylcholine release in muscle cells.

Effect of lanthanum ions on function and structure of frog neuromuscular junctions

Lanthanum ions activate transmitter release in frog neuromuscular junctions, increasing transmitter release without presynaptic membrane depolarization, but without affecting nerve terminal structure.

New step in transmitter release at the myoneural junction.

Acetylcholine release from vesicles in neuromuscular synapses involves a complex process involving calcium influx, electrical field changes, and calcium-dependent protein phosphorylation.

A comparison of the effects of various sulfhydryl reagents on neuromuscular transmission.

Sulfhydryl reagents can block neuromuscular transmission, causing muscle contraction and depression, with some showing specific effects depending on their lipid solubility.

Citations