Cultured Schwann cells are characterized by a strong outward rectification of the membrane; the threshold of the outward currents is close to the resting membrane potential of about -50 mV (Gray et al.: In Ritchie, Keynes (eds): Ion Channels in Neural Membranes. New York: Alan R. Liss, Inc., pp 145-
K+ channel properties in cultured mouse Schwann cells: Dependence on extracellular K+
✍ Scribed by A. Verkhratsky; D. Hoppe; Dr. H. Kettenmann
- Publisher
- John Wiley and Sons
- Year
- 1991
- Tongue
- English
- Weight
- 493 KB
- Volume
- 28
- Category
- Article
- ISSN
- 0360-4012
No coin nor oath required. For personal study only.
✦ Synopsis
In cultured Schwann cells, single-channel and whole-cell K+ currents can be activated by depolarizing the membrane to values more negative than -50 mV. In elevated extracellular K+ concentration ([K+]o), however, single-channel activity and whole-cell currents could be recorded at more negative potentials. Thus, the threshold of current activation was shifted to more negative potentials. This shift in the activation threshold was only observed with normal (50-60 mM) intracellular [K+] levels; it was not apparent when [K+]i was elevated to 145 mM. The control of [K+]o on the gating properties of K+ channels may serve to enhance the capability of the Schwann cell to take up [K+]o and thus may serve for [K+] homeostasis in the peripheral nerve.
📜 SIMILAR VOLUMES
## Abstract The endogenous Mg^2+^‐inhibited cation (MIC) current was recently described in different cells of hematopoietic lineage and was implicated in the regulation of Mg^2+^ homeostasis. Here we present a single channel study of endogenously expressed Mg^2+^‐dependent cation channels in the hu
## Abstract The Trembler‐J (TrJ) mouse, containing a point mutation in the peripheral myelin protein 22 gene, is characterized by severe hypomyelination and is a representative model of Charcot‐Marie‐Tooth 1A disease/Dejerine‐Sottas Syndrome. Previous studies have shown that protein kinase inhibito
It is well established that neurons regulate the properties of both central and peripheral glial cells. Some of these neuro-glial interactions are modulated by the pattern of neuronal electrical activity. In the present work, we asked whether blocking the electrical activity of dorsal root ganglion