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The Influence of External Potassium on the Inactivation of Sodium Currents in the Giant Axon of the Squid, Loligo pealei
Isolated giant axons were voltage-clamped in seawater solutions having constant sodium concentrations of 230 mM and variable potassium concentrations of from zero to 210 mM. The inactivation of the initial transient membrane current normally carried by Na(+) was studied by measuring the Hodgkin-Huxl...
Autores principales: | , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
The Rockefeller University Press
1969
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2202877/ https://www.ncbi.nlm.nih.gov/pubmed/5783008 |
Sumario: | Isolated giant axons were voltage-clamped in seawater solutions having constant sodium concentrations of 230 mM and variable potassium concentrations of from zero to 210 mM. The inactivation of the initial transient membrane current normally carried by Na(+) was studied by measuring the Hodgkin-Huxley h parameter as a function of time. It was found that h reaches a steady-state value within 30 msec in all solutions. The values of h (∞), τ(h), α(h),and β(h) as functions of membrane potential were determined for various [K (o)]. The steady-state values of the h parameter were found to be inversely related, while the time constant, τ(h), was directly related to external K(+) concentration. While the absolute magnitude as well as the slopes of the h (∞) vs. membrane potential curves were altered by varying external K(+), only the magnitude and not the shape of the corresponding τ(h) curves was altered. Values of the two rate constants, α(h) and β(h), were calculated from h(∞) and τ(h) values. α(h) is inversely related to [K(o)] while β(h) is directly related to [K(o)] for hyperpolarizing membrane potentials and is independent of [K(o)] for depolarizing membrane potentials. Hodgkin-Huxley equations relating α(h) and β(h) to E(m) were rewritten so as to account for the observed effects of [K(o)]. It is concluded that external potassium ions have an inactivating effect on the initial transient membrane conductance which cannot be explained solely on the basis of potassium membrane depolarization. |
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