Activity-dependent regulation of inwardly rectifying potassium currents in non-myelinating Schwann cells in mice.
1. Voltage-gated potassium currents were recorded from freshly dissociated non-myelinating Schwann cells of sural and sympathetic nerves from 1- to 12-week-old mice using the whole-cell or a single channel variation of the patch-clamp technique. 2. All sural cells from 2-week-old mice showed inwardly rectifying potassium (Kir+) currents in whole-cell recordings. Kir+ currents were virtually undetectable in sural cells from mice more than 6 weeks old, which also showed depolarization of the resting membrane potential. On the other hand, the magnitude of Kir+ currents increased in cervical sympathetic trunk (CST) cells in parallel with an increase of cell capacitance 1-6 weeks after birth. The density of Kir+ currents in CST cells increased 1-4 weeks after birth and then stayed constant for up to 12 weeks. 3. The unitary conductance of a single Kir+ channel in CST cells was 30 pS 2-12 weeks after birth; this was recorded in a cell-attached configuration with 154 mM K+ in the pipette. The steady-state open channel probability of single Kir+ channels in CST cells decreased with membrane hyperpolarization, but was not markedly changed 2-12 weeks after birth. 4. Conduction block of CST for 5 days induced by local application of tetrodotoxin (TTX) resulted in a significant decrease in both the magnitude and the density of Kir+ currents in whole-cell recordings in CST cells rostral to the sites of TTX block. Similar changes of Kir+ currents in whole-cell recordings were observed in cells in the inferior postganglionic branch of a superior cervical ganglion after 5 days of TTX block of CST. 5. These results suggest that neuronal activity regulates the expression of functional Kir+ channels in non-myelinating Schwann cells in adult nerves. The activity-dependent regulation of the expression of glial potassium channels could play an important role in the regulation of the potassium microenvironment around active axons to maintain impulse conduction in unmyelinated fibres.
Konishi
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Department of Neurology, Utano National Hospital, Kyoto, Japan.
D000375:Aging / Q000378:metabolism; D000818:Animals; D001464:Barium / Q000494:pharmacology; D004594:Electrophysiology; D015640:Ion Channel Gating / Q000502:physiology*; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D051379:Mice; D008807:Mice, Inbred BALB C; D009186:Myelin Sheath / Q000502:physiology; D009412:Nerve Fibers / Q000187:drug effects / Q000502:physiology*; D009431:Neural Conduction / Q000187:drug effects; D015221:Potassium Channels / Q000187:drug effects / Q000502:physiology*; D011803:Quinine / Q000494:pharmacology; D012583:Schwann Cells / Q000187:drug effects / Q000502:physiology*; D013497:Sural Nerve / Q000166:cytology / Q000254:growth & development / Q000502:physiology; D013564:Sympathetic Nervous System / Q000166:cytology / Q000254:growth & development / Q000502:physiology; D013779:Tetrodotoxin / Q000494:pharmacology
D015221:Potassium Channels; D001464:Barium; D013779:Tetrodotoxin; D011803:Quinine