Slow inactivation of the sodium conductance in squid giant axons. Pronase resistance.

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Destruction of Sodium Conductance Inactivation in Squid Axons Perfused with Pronase

We have studied the effects of the proteolytic enzyme Pronase on the membrane currents of voltage-clamped squid axons. Internal perfusion of the axons with Pronase rather selectively destroys inactivation of the Na conductance (g(Na)). At the level of a single channel, Pronase probably acts in an all-or-none manner: each channel inactivates normally until its inactivation gate is destroyed, and...

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Sodium Movements in Perfused Squid Giant Axons

Sodium movements in internally perfused giant axons from the squid Dosidicus gigas were studied with varying internal sodium concentrations and with fluoride as the internal anion. It was found that as the internal concentration of sodium was increased from 2 to 200 mM the resting sodium efflux increased from 0.09 to 34.0 pmoles/cm(2)sec and the average resting sodium influx increased from 42.9...

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Removal of sodium channel inactivation in squid giant axons by n- bromoacetamide

The group-specific protein reagents, N-bromacetamide (NBA) and N-bromosuccinimide (NBS), modify sodium channel gating when perfused inside squid axons. The normal fast inactivation of sodium channels is irreversibly destroyed by 1 mM NBA or NBS near neutral pH. NBA apparently exhibits an all-or-none destruction of the inactivation process at the single channel level in a manner similar to inter...

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Remo, al of Sodium Channel Inactivation in Squid Giant Axons by N-Bromoacetamide

The group-specific protein reagents, N-bromoacetamide (NBA) and N-bromosuccinimide (NBS), modify sodium channel gating when perfused inside squid axons. The normal fast inactivation of sodium channels is irreversibly destroyed by 1 mM NBA or NBS near neutral pH. NBA apparently exhibits an allor-none destruction of the inactivation process at the single channel level in a manner similar to inter...

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On the persistent sodium current in squid giant axons.

R. F. Rakowski, D. C. Gadsby, and P. DeWeer have reported a persistent, tetrodotoxin-sensitive sodium ion current (I(NaP)) in squid giant axons having a low threshold (-90 mV) and a maximal inward amplitude of -4 microA/cm(2) at -50 mV. This report makes the case that most of I(NaP) is attributable to an ion channel mechanism distinct from the classical rapidly activating and inactivating sodiu...

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ژورنال

عنوان ژورنال: The Journal of Physiology

سال: 1978

ISSN: 0022-3751

DOI: 10.1113/jphysiol.1978.sp012485