We studied the distribution of voltage-gated Ca2+ channels in cells of
the oligodendrocyte lineage from retinal and cortical cultures. Influ
x of Ca2+ via voltage-gated channels was activated by membrane depolar
ization with elevated extracellular K+ concentration ([K+](e)) and loc
al, subcellular increases in cytosolic free Ca2+ concentration ([Ca2+]
(i)n) could be monitored with a fluometric system connected to a laser
scanning confocal microscope. In glial precursor cells from both reti
na and cortex, small depolarizations (with 10 or 20 mM K+) activated C
a2+ transients in processes indicating the presence of low-voltage-act
ivated Ca2+ channels. Larger depolarizations (with 50 mM K+) additiona
lly activated high-voltage-activated Ca2+ channels in the soma. An une
ven distribution of Ca2+ channels was also observed in the mature olig
odendrocytes; Ca2+ transients in processes were considerably larger. R
ecovery of Ca2+ levels after the voltage-induced influx was achieved b
y the activity of the plasmalemmal Ca2+ pump, while mitochondria playe
d a minor role to restore Ca2+ levels after an influx through voltage-
operated channels. During the development of white matter tracts, cell
s of the oligodendrocyte lineage contact axons to form myelin. Neurona
l activity is accompanied by increases in [K+](e); this may lead to Ca
2+ changes in the processes and the Ca2+ increase might be a signal fo
r the glial precursor cell to start myelin formation. (C) 1995 Wiley-L
iss, Inc.