Voltage-dependent calcium and potassium channels in Schwann cells cultured from dorsal root ganglia of the mouse.
1. Whole-cell patch clamp studies were carried out on Schwann cells in organotypic cultures of dorsal root ganglia (DRG) from OF1 mice embryos (18-19 days). 2. In standard external solution, from a holding potential of -70 mV, two types of voltage-dependent K+ currents were recorded: a fast transient current and a delayed sustained current. With a holding potential of -30 mV, only the delayed sustained current could be evoked. 3. Both K+ currents were inhibited by tetraethylammonium chloride (TEA) and 4-aminopyridine (4-AP) in a dose-dependent manner. For the transient current the half-maximal effective dose was 100 mM for TEA and 1.3 mM for 4-AP. For the delayed sustained current the half-maximal effective dose was 11 mM for TEA and 4 mM for 4-AP. Both currents were insensitive to external Ca2+. 4. The delayed sustained current, isolated by use of a holding potential of -30 mV displayed a 'cumulative inactivation' which was removed by hyperpolarizing the membrane to -70 mV between each test pulse. 5. In K(+)-free external and pipette solutions, with 10 mM-external Ca2+, from a holding potential of -70 mV voltage-dependent Ca2+ channel currents were recorded. The threshold for activation was -45.3 +/- 5.4 mV (mean +/- S.D., n = 5) and the current inactivated fully at the end of the test potential. The current was unaffected by 2 microM-tetrodotoxin (TTX) and totally blocked by 5 mM-Co2+. 6. Equimolar replacement of external Ca2+ by Ba2+ did not significantly modify the voltage dependence (threshold for activation -42.8 +/- 6.4 mV, n = 7) or the magnitude of the inward current. Ca2+ and Ba2+ were equally permeant. The fully inactivating current was insensitive to both nifedipine and Bay K 8644 (1 microM each). Increasing the external Ba2+ concentration from 10 to 89 mM enhanced the Ba2+ current and shifted the voltage dependence of the current (threshold for activation, -30.5 +/- 7.3 mV, n = 9) along the voltage axis as expected for altered external surface potential. 7. In 89 mM-external Ba2+ solution, some cells displayed an additional slowly decaying current which was totally blocked by nifedipine (1 microM). 8. Ca2+ channel currents were recorded only when DRG neurons were present in the culture, as excision of explants and subsequent axonal degeneration led to loss of detectable Ca2+ channel currents. This phenomenon was never observed for K+ currents. 9. We conclude that mouse Schwann cells in organotypic culture possess voltage-dependent K+ and Ca2+ channels.(ABSTRACT TRUNCATED AT 400 WORDS)
Amédée
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Institut National de la Santé et de la Recherche Médicale, Unité de Neurobiologie Intégrative, Bordeaux, France.
Ellie
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Dupouy
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Vincent
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JD
D015761:4-Aminopyridine / Q000494:pharmacology; D000818:Animals; D001464:Barium / Q000378:metabolism; D015220:Calcium Channels / Q000187:drug effects / Q000502:physiology*; D002478:Cells, Cultured; D003035:Cobalt / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D005727:Ganglia, Spinal / Q000166:cytology; D008564:Membrane Potentials / Q000187:drug effects; D051379:Mice; D009543:Nifedipine / Q000494:pharmacology; D015221:Potassium Channels / Q000187:drug effects / Q000502:physiology*; D012583:Schwann Cells / Q000502:physiology*; D019789:Tetraethylammonium; D013757:Tetraethylammonium Compounds / Q000494:pharmacology; D013779:Tetrodotoxin / Q000494:pharmacology
D015220:Calcium Channels; D015221:Potassium Channels; D013757:Tetraethylammonium Compounds; D001464:Barium; D003035:Cobalt; D013779:Tetrodotoxin; D019789:Tetraethylammonium; D015761:4-Aminopyridine; D009543:Nifedipine