## Abstract Loss of axons is a major contributor to nonremitting deficits in the inflammatory demyelinating disease multiple sclerosis (MS). Based on biophysical studies showing that activity of axonal sodium channels can trigger axonal degeneration, recent studies have tested sodium channel‐blocki
Sodium channel in isolated human brain macrophages (microglia)
✍ Scribed by Wolfgang Nöurenberg; Peter Illes; Peter J. Gebicke-Haerter
- Publisher
- John Wiley and Sons
- Year
- 1994
- Tongue
- English
- Weight
- 799 KB
- Volume
- 10
- Category
- Article
- ISSN
- 0894-1491
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
Human brain macrophages (microglia) have been isolated from mixed brain cell cultures initiated from explants of neurosurgical adult human tissue in one step according to a method developed for rat microglia. Cells were characterized enzyme‐histochemically (NDPase) in mixed and immunocytochemically (anti‐CD 14) in mixed and isolated cultures. Purified cells were used to investigate in more detail membrane currents by the patch clamp technique. In 14 cells microdialyzed with a standard, K^+^‐containing intracellular solution there was no indication for a hyperpolarization‐induced K^+^‐inward current characteristic for newborn rat microglia. However, in 12 cells depo‐larizing pulses initiated a rapidly inactivating inward current which was followed by an outward current (in 4 cells). The outward current appeared to be carried by K^+^, since it was absent in another 18 cells, recorded by micropipettes containing Cs^+^ instead of K^+^ as the main intracellular cation. The depolarization‐induced inward current persisted un‐der these conditions. This current was inhibited by tetrodotoxin (5μM) and by substitu‐tion of Na^+^ by choline in the bath solution. It is suggested that this Na^+^‐current is specifically expressed in macrophages derived from adult brain. © 1994 Wiley‐Liss, Inc.
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