Premium
Subcellular heterogeneity of voltage‐gated Ca 2+ channels in cells of the oligodendrocyte lineage
Author(s) -
Kirischuk S.,
Scherer J.,
Möller T.,
Verkhratsky A.,
Kettenmann H.
Publication year - 1995
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.440130102
Subject(s) - oligodendrocyte , depolarization , biology , myelin , soma , biophysics , membrane potential , voltage gated ion channel , microbiology and biotechnology , extracellular , ion channel , neuroscience , biochemistry , central nervous system , receptor
We studied the distribution of voltage‐gated Ca 2+ channels in cells of the oligodendrocyte lineage from retinal and cortical cultures. Influx Of ca 2+ via voltagegated channels was activated by membrane depolarization with elevated extracellular K + concentration ([K + ] e ) and local, subcellular increases in cytosolic free Ca 2+ concentration ([Ca 2+ ] in ) could be monitored with a fluometric system connected to a laser scanning confocal microscope. In glial precursor cells from both retina and cortex, small depolarizations (with 10 or 20 mM K + ) activated Ca 2+ transients in processes indicating the presence of low‐voltage‐activated Ca 2+ channels. Larger depolarizations (with 50 mM K + ) additionally activated high‐voltage‐activated Ca 2+ channels in the soma. An uneven distribution of Ca 2+ channels was also observed in the mature oligodendrocytes; Ca 2+ trasients in processes were considerably larger. Recovery of Ca 2+ levels after the voltage‐induced influx was achieved by the activity of the plasmalemmal Ca 2+ pump, while mitochondria played a minor role to restore 2+ levels after an influx through voltageoperated channels. During the development of white matter tracts, cells of the oligodendrocyte lineage contact axons to form myelin. Neuronal activity is accompanied by increases in [K + ] e ; this may lead to Ca 2+ changes in the processes and the Ca 2+ increase might be a signal for the glial precursor cell to start myelin formation. © 1995 Wiley‐Liss, Inc.