Changes in excitable membrane properties in Schwann cells of adult rabbit sciatic nerves following nerve transection.

摘要

1. Whole-cell patch clamp studies were carried out on Schwann cells associated with myelinated and non-myelinated axons in the distal nerve stump of transected adult rabbit sciatic nerves which had undergone in vivo degeneration for 0-13 days. 2. Voltage-gated sodium current of Schwann cells associated with non-myelinated axons decreased in amplitude following nerve transection; the peak current density decreased to about 51% by day 3, and to 27% by day 6. The number of non-myelinated axons, determined from cross-sectional electron microscopy of the whole nerve bundle, also exhibited a similar decline to 48% (day 3) and 17% (day 6) of the control values. 3. In contrast, both voltage-gated sodium and potassium currents of Schwann cells associated with myelinated axons showed an increase following nerve transection. These two currents, normally not detectable in these Schwann cells, first appeared at around day 4 after nerve transection and increased progressively with time thereafter as Wallerian degeneration persisted. 4. The whole-cell membrane capacity of Schwann cells also exhibited different pattern of changes, depending on whether the cell normally lacked or produced myelin. In the former, the cell capacity remained relatively constant following nerve transection. In the latter, the whole cell capacity was reduced to 11% of control values by day 13. This capacity decline is consistent with the observed detachment of myelin membranes from these latter Schwann cells. 5. There was an apparent inverse relation between the whole-cell capacity and the density of sodium and potassium currents in Schwann cells undergoing progressive myelin loss. It is suggested that the appearance of sodium and potassium currents in these cells might be related to myelin degeneration. 6. A hypothesis is proposed that the expression of excitable ion channels (sodium and potassium) on a Schwann cell is under opposing regulation by degenerating myelin and by axons. Axonal degeneration leads to a decline of Schwann cell sodium currents. Myelin degeneration, in contrast, leads to an increase of both Schwann cell sodium and potassium currents. 7. The above hypothesis that axons normally exert a positive trophic influence on Schwann cells to express sodium channels is discussed in relation to a recent speculation of a Schwann-to-axon transfer of excitable ion channels.