Deutsch
 
Hilfe Datenschutzhinweis Impressum
  DetailsucheBrowse

Datensatz

DATENSATZ AKTIONENEXPORT

Freigegeben

Zeitschriftenartikel

Na(+)-activated K+ channels localized in the nodal region of myelinated axons of Xenopus

MPG-Autoren
/persons/resource/persons93833

Koh,  Duk Su
Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society;

/persons/resource/persons93625

Jonas,  Peter
Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society;

Volltexte (beschränkter Zugriff)
Für Ihren IP-Bereich sind aktuell keine Volltexte freigegeben.
Volltexte (frei zugänglich)
Es sind keine frei zugänglichen Volltexte in PuRe verfügbar
Ergänzendes Material (frei zugänglich)
Es sind keine frei zugänglichen Ergänzenden Materialien verfügbar
Zitation

Koh, D. S., Jonas, P., & Vogel, W. (1994). Na(+)-activated K+ channels localized in the nodal region of myelinated axons of Xenopus. The Journal of Physiology - London, 479(2), 183-197. doi:10.1113/jphysiol.1994.sp020287.


Zitierlink: https://hdl.handle.net/11858/00-001M-0000-0019-A8CB-6
Zusammenfassung
A potassium channel activated by internal Na+ ions (K+Na channel) was identified in peripheral myelinated axons of Xenopus laevis using the cell−attached and excised configurations of the patch clamp technique. 2. The single−channel conductance for the main open state was 88 pS with [K+]o = 105 mM and pS with [K+]o = 2.5 mM ([K+]i = 105 mM). The channel was selectively permeable to K+ over Na+ ions. A characteristic feature of the K+Na channel was the frequent occurrence of subconductance states. 3. The open probability of the channel was strongly dependent on the concentration of Na+ ions at the inner side of the membrane. The half−maximal activating Na+ concentration and the Hill coefficient were 33 mM and 2.9, respectively. The open probability of the channel showed only weak potential dependence. 4. The K+Na channel was relatively insensitive to external tetraethylammonium (TEA+) in comparison with voltage−dependent axonal K+ channels; the half−maximal inhibitory concentration (IC50) was 21.3 mM (at −90 mV). In contrast, the channel was blocked by low concentrations of external Ba2+ and Cs+ ions, with IC50 values of 0.7 and 1.1 mM, respectively (at −90 mV). The block by Ba2+ and Cs+ was more pronounced at negative than at positive membrane potentials. 5. A comparison of the number of K+Na channels in nodal and paranodal patches from the same axon revealed that the channel density was about 10−fold higher at the node of Ranvier than at the paranode. Moreover, a correlation between the number of K+Na channels and voltage−dependent Na+ channels in the same patches was found, suggesting co−localization of both channel types. 6. As weakly potential−dependent ('leakage') channels, axonal K+Na channels may be involved in setting the resting potential of vertebrate axons. Simulations of Na+ ion diffusion suggest two possible mechanisms of activation of K+Na channels: the local increase of Na+ concentration in a cluster of Na+ channels during a single action potential or the accumulation in the intracellular axonal compartment during a train of action potentials