title: Voltage-gated potassium currents in myelinating Schwann cells in the mouse.
abstract: 1. The whole-cell variation of the patch-clamp technique was used to record ionic currents in Schwann cells obtained from enzyme-treated mouse sciatic nerves before and after the onset of myelination. 2. Only outward currents were evoked in embryonic Schwann cells, which had no myelin, at membrane potentials more positive than -40 mV. Neonatal myelinating cells developed depolarization-activated outward currents and hyperpolarization-activated inward currents. For large hyperpolarizations below -160 mV, inward currents exhibited a sag following a peak which appeared to be mainly due to Na+ blockade. 3. Membrane potentials of neonatal myelinating cells were more negative than those of embryonic cells. The depolarization of the membrane potentials per 10-fold increase in external K+ concentrations in neonatal myelinating cells was 57 mV which fits the Nernst equation for a K+ electrode. 4. Quinine (0.5-2 mM) blocked the outward currents in embryonic cells and Ba2+ (2 mM) blocked both outward and inward currents in neonatal myelinating cells leaving quinine-sensitive outward currents of the embryonic type. External Cs+ (5 mM) blocked mainly inward currents and internal Cs+ blocked outward currents. 5. Developmental changes of these voltage-gated K+ currents in myelinating cells showed that Ba2(+)-sensitive K+ currents disappeared rapidly during the first week of life in association with the membrane potential becoming more positive. In contrast, quinine-sensitive outward K+ currents of the embryonic type disappeared slowly during the first 3-4 weeks after birth. 6. It is concluded that neonatal myelinating Schwann cells developed new voltage-gated K+ channels, which are Ba2(+)-sensitive and set a new membrane potential, in addition to the voltage-gated K+ channels of embryonic type. The Ba2(+)-sensitive K+ channels in myelinating cells were suggested to play an important role in siphoning K+ ions accumulated in periaxonal space during nerve activities.
authors.affiliation: Department of Neurology, Utano National Hospital, Kyoto, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Konishi
mesh_terms: D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D000831:Animals, Newborn; D001464:Barium / Q000494:pharmacology; D002586:Cesium / Q000494:pharmacology; D066298:In Vitro Techniques; D015640:Ion Channel Gating / Q000502:physiology*; D008564:Membrane Potentials / Q000502:physiology; D051379:Mice; D008810:Mice, Inbred C57BL; D009186:Myelin Sheath / Q000502:physiology*; D011188:Potassium / Q000502:physiology*; D015221:Potassium Channels / Q000502:physiology; D011803:Quinine / Q000494:pharmacology; D012583:Schwann Cells / Q000502:physiology*; D012584:Sciatic Nerve / Q000196:embryology / Q000502:physiology; D012964:Sodium / Q000494:pharmacology
chemical_list: D015221:Potassium Channels; D002586:Cesium; D001464:Barium; D012964:Sodium; D011803:Quinine; D011188:Potassium