Hg2+ causes neurotoxicity at an intracellular site following entry through Na and Ca channels
| Autor: | Michael D. Miyamoto |
|---|---|
| Rok vydání: | 1983 |
| Předmět: |
Neuromuscular Junction
Motor nerve Tetrodotoxin Motor Endplate Synaptic Transmission Neuromuscular junction Ion Channels Pectoralis Muscles chemistry.chemical_compound medicine Animals Channel blocker Molecular Biology Irreversible Toxicity General Neuroscience Rana pipiens Sodium Neurotoxicity Depolarization Cobalt medicine.disease medicine.anatomical_structure chemistry Anesthesia Mercury Poisoning Biophysics Calcium Neurology (clinical) Intracellular Developmental Biology |
| Zdroj: | Brain research. 267(2) |
| ISSN: | 0006-8993 |
| Popis: | At motor nerve terminals, Hg 2+ causes (a) irreversible depolarization, (b) increase in transmitter release, and (c) subsequent irreversible block of transmitter release. All effects are antagonized when a Na channel blocker (tetrodotoxin, TTX) and a Ca channel blocker (Co 2+ ) are present, but not when either blocker is used alone. The effects are not antagonized by TTX plus Co 2+ when the mercurial is lipid-soluble (methylmercury). This indicates that the neurotoxic action of Hg 2+ is at an intracellular site and that entry is gained through both Na and Ca channels. The results suggest that metals may inhibit transmitter release at either the Ca channel or at the release site, but that irreversible toxicity is due to an intracellular action, possibly involving SH groups. |
| Databáze: | OpenAIRE |
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