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

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

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

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Citation

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.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0019-A8CB-6
Abstract
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