Abstract
The effects of tetraethylammonium and manganese, which modify calcium entry into motor nerve terminals, have been studied during advanced stages of botulinum paralysis. Evidence has been obtained that the voltage-activated calcium current in the nerve endings is not significantly reduced by botulinum toxin. The depression of transmitter release that the toxin produces must arise at a later stage, at an intracellular site of the release mechanism.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Acetylcholine / metabolism
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Action Potentials / drug effects
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Animals
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Botulinum Toxins / pharmacology*
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Calcium / antagonists & inhibitors*
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Manganese / pharmacology
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Nerve Endings / drug effects
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Neuromuscular Junction / drug effects*
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Rana temporaria
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Secretory Rate / drug effects
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Tetraethylammonium Compounds / pharmacology
Substances
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Tetraethylammonium Compounds
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Manganese
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Botulinum Toxins
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Acetylcholine
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Calcium