Selective modification of sodium channel gating in lobster axons by 2,4,6 trinitrophenol. Evidence for two inactivation mechanisms

G. S. Oxford, J. P. Pooler

Research output: Contribution to journalArticle

31 Citations (Scopus)

Abstract

Trinitrophenol (TNP) selectively alters the sodium conductance system of lobster giant axons as measured in current clamp and voltage clamp experiments using the double sucrose gap technique. TNP has no measurable effect on potassium currents but reversibly prolongs the time course of sodium currents during maintained depolarizations over the full voltage range of observable currents. Action potential durations are increased also. T(m) of the Hodgkin Huxley model is not markedly altered during activation of the sodium conductance but is prolonged during removal of activation by repolarization, as observed in sodium tail experiments. The sodium inactivation versus voltage curve is shifted in the hyperpolarizing direction as is the inactivation time constant curve, measured with conditioning voltage steps. This shift speeds the kinetics of inactivation over part of the same voltage range in which sodium currents are prolonged, a contradiction incompatible with the Hodgkin Huxley model. These results are interpreted as support for a hypothesis of two inactivation processes, one proceeding directly from the resting state and the other coupled to the active state of sodium conductance.

Original languageEnglish (US)
Pages (from-to)765-779
Number of pages15
JournalJournal of General Physiology
Volume66
Issue number6
StatePublished - 1975
Externally publishedYes

Fingerprint

Sodium Channels
Axons
Sodium
picric acid
Action Potentials
Sucrose
Potassium

ASJC Scopus subject areas

  • Physiology

Cite this

Selective modification of sodium channel gating in lobster axons by 2,4,6 trinitrophenol. Evidence for two inactivation mechanisms. / Oxford, G. S.; Pooler, J. P.

In: Journal of General Physiology, Vol. 66, No. 6, 1975, p. 765-779.

Research output: Contribution to journalArticle

@article{4461f9aab5e74a2ca0218a5b06eae534,
title = "Selective modification of sodium channel gating in lobster axons by 2,4,6 trinitrophenol. Evidence for two inactivation mechanisms",
abstract = "Trinitrophenol (TNP) selectively alters the sodium conductance system of lobster giant axons as measured in current clamp and voltage clamp experiments using the double sucrose gap technique. TNP has no measurable effect on potassium currents but reversibly prolongs the time course of sodium currents during maintained depolarizations over the full voltage range of observable currents. Action potential durations are increased also. T(m) of the Hodgkin Huxley model is not markedly altered during activation of the sodium conductance but is prolonged during removal of activation by repolarization, as observed in sodium tail experiments. The sodium inactivation versus voltage curve is shifted in the hyperpolarizing direction as is the inactivation time constant curve, measured with conditioning voltage steps. This shift speeds the kinetics of inactivation over part of the same voltage range in which sodium currents are prolonged, a contradiction incompatible with the Hodgkin Huxley model. These results are interpreted as support for a hypothesis of two inactivation processes, one proceeding directly from the resting state and the other coupled to the active state of sodium conductance.",
author = "Oxford, {G. S.} and Pooler, {J. P.}",
year = "1975",
language = "English (US)",
volume = "66",
pages = "765--779",
journal = "Journal of General Physiology",
issn = "0022-1295",
publisher = "Rockefeller University Press",
number = "6",

}

TY - JOUR

T1 - Selective modification of sodium channel gating in lobster axons by 2,4,6 trinitrophenol. Evidence for two inactivation mechanisms

AU - Oxford, G. S.

AU - Pooler, J. P.

PY - 1975

Y1 - 1975

N2 - Trinitrophenol (TNP) selectively alters the sodium conductance system of lobster giant axons as measured in current clamp and voltage clamp experiments using the double sucrose gap technique. TNP has no measurable effect on potassium currents but reversibly prolongs the time course of sodium currents during maintained depolarizations over the full voltage range of observable currents. Action potential durations are increased also. T(m) of the Hodgkin Huxley model is not markedly altered during activation of the sodium conductance but is prolonged during removal of activation by repolarization, as observed in sodium tail experiments. The sodium inactivation versus voltage curve is shifted in the hyperpolarizing direction as is the inactivation time constant curve, measured with conditioning voltage steps. This shift speeds the kinetics of inactivation over part of the same voltage range in which sodium currents are prolonged, a contradiction incompatible with the Hodgkin Huxley model. These results are interpreted as support for a hypothesis of two inactivation processes, one proceeding directly from the resting state and the other coupled to the active state of sodium conductance.

AB - Trinitrophenol (TNP) selectively alters the sodium conductance system of lobster giant axons as measured in current clamp and voltage clamp experiments using the double sucrose gap technique. TNP has no measurable effect on potassium currents but reversibly prolongs the time course of sodium currents during maintained depolarizations over the full voltage range of observable currents. Action potential durations are increased also. T(m) of the Hodgkin Huxley model is not markedly altered during activation of the sodium conductance but is prolonged during removal of activation by repolarization, as observed in sodium tail experiments. The sodium inactivation versus voltage curve is shifted in the hyperpolarizing direction as is the inactivation time constant curve, measured with conditioning voltage steps. This shift speeds the kinetics of inactivation over part of the same voltage range in which sodium currents are prolonged, a contradiction incompatible with the Hodgkin Huxley model. These results are interpreted as support for a hypothesis of two inactivation processes, one proceeding directly from the resting state and the other coupled to the active state of sodium conductance.

UR - http://www.scopus.com/inward/record.url?scp=0016797437&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0016797437&partnerID=8YFLogxK

M3 - Article

C2 - 1194889

AN - SCOPUS:0016797437

VL - 66

SP - 765

EP - 779

JO - Journal of General Physiology

JF - Journal of General Physiology

SN - 0022-1295

IS - 6

ER -