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PMID: 26973 Published · ppublish English Journal Article Research Support, U.S. Gov't, P.H.S.

Sodium channel inactivation in squid axon is removed by high internal pH or tyrosine-specific reagents.

Science (New York, N.Y.) ·Vol. 200 ·No. 4349 ·1978-06-30 ·Pages 1494-6

Brodwick MS, Eaton DC

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.

MeSH Terms

Animals Axons/metabolism Biological Transport/drug effects Cell Membrane Permeability/drug effects Decapodiformes Electric Conductivity Hydrogen Bonding Hydrogen-Ion Concentration In Vitro Techniques Iodides/metabolism Lactoperoxidase/metabolism Sodium/metabolism Tetranitromethane/pharmacology Tyrosine/antagonists & inhibitors

Chemicals

Iodides Tyrosine Sodium Lactoperoxidase Tetranitromethane

Authors & Affiliations

2 authors, click to expand affiliations / ORCID

Brodwick M S

Eaton D C

Article Info

Journal

Science (New York, N.Y.)

Abbr.

Science

ISSN

0036-8075

DOI

10.1126/science.26973

Published

1978-06-30

Pages

1494-6

Language

English

Region

United States

NLM ID

0404511

Subset

External Links

PubMed source DOI: 10.1126/science.26973 View journal details

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Sodium channel inactivation in squid axon is removed by high internal pH or tyrosine-specific reagents.

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