Na(+)-activated K+ channels localized in the nodal region of myelinated axons of Xenopus.
1. 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.
Koh
D S
DS
Physiologisches Institut, Justus-Liebig-Universität, Giessen, Germany.
Jonas
P
P
Vogel
W
W
D000818:Animals; D001369:Axons / Q000187:drug effects / Q000378:metabolism* / Q000648:ultrastructure; D001464:Barium / Q000494:pharmacology; D002463:Cell Membrane Permeability; D002586:Cesium / Q000494:pharmacology; D003711:Demyelinating Diseases / Q000139:chemically induced / Q000378:metabolism; D007150:Immunohistochemistry; D008564:Membrane Potentials; D008854:Microscopy, Electron; D009186:Myelin Sheath / Q000187:drug effects / Q000378:metabolism / Q000648:ultrastructure; D018408:Patch-Clamp Techniques; D026902:Potassium Channel Blockers; D015221:Potassium Channels / Q000187:drug effects / Q000378:metabolism*; D011901:Ranvier's Nodes / Q000187:drug effects / Q000378:metabolism / Q000648:ultrastructure*; D012964:Sodium / Q000378:metabolism*; D015222:Sodium Channels / Q000378:metabolism; D019789:Tetraethylammonium; D013757:Tetraethylammonium Compounds / Q000494:pharmacology; D014982:Xenopus laevis
D026902:Potassium Channel Blockers; D015221:Potassium Channels; D015222:Sodium Channels; D013757:Tetraethylammonium Compounds; D002586:Cesium; D001464:Barium; D019789:Tetraethylammonium; D012964:Sodium