Abstract
In squid axon, internal alkalinization from pH 7.1 to pH 10.2 results in a reversible decrease of the maximum inward current and the steady state sodium channel inactivation. Similar effects were observed after treatment of the axon with tetranitromethane or after iodination with lactoperoxidase. These results suggest that a tyrosine residue is an essential component of the inactivation process in this nerve.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Axons / metabolism*
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Biological Transport / drug effects
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Cell Membrane Permeability / drug effects
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Decapodiformes
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Electric Conductivity
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Hydrogen Bonding
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Hydrogen-Ion Concentration
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In Vitro Techniques
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Iodides / metabolism
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Lactoperoxidase / metabolism
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Sodium / metabolism*
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Tetranitromethane / pharmacology
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Tyrosine / antagonists & inhibitors*
Substances
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Iodides
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Tyrosine
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Sodium
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Lactoperoxidase
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Tetranitromethane