Sodium Channel Inactivation in Squid Axon is Removed by High Internal pH or Tyrosine-Specific Reagents

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. Th...

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Bibliographic Details
Published in:Science (American Association for the Advancement of Science) 1978-06, Vol.200 (4349), p.1494-1496
Main Authors: Brodwick, Malcolm S., Eaton, Douglas C.
Format: Article
Language:English
Subjects:
Animals
Axons
Axons - metabolism
Biological Transport - drug effects
Cell Membrane Permeability - drug effects
Cystic fibrosis
Decapodiformes
DNA damage
Electric Conductivity
Electric potential
Hydrogen Bonding
Hydrogen-Ion Concentration
In Vitro Techniques
Iodides - metabolism
Lactoperoxidase - metabolism
Reagents
Sodium
Sodium - metabolism
Sodium channels
Spores
Tetranitromethane - pharmacology
Tyrosine - antagonists & inhibitors
Urine
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Summary: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.
ISSN:0036-8075
1095-9203
DOI:10.1126/science.26973