AJP - Cell Physiology, Vol 264, Issue 3 C632-C640, Copyright © 1993 by American Physiological Society

ARTICLES

Arachidonic acid and its metabolites increase Cai in cultured rat oligodendrocytes

B. Soliven, M. Takeda, T. Shandy and D. J. Nelson
Department of Neurology, University of Chicago, Illinois 60637.

Fluorescence measurements of intracellular calcium (Cai) were made on cultured rat spinal cord oligodendrocytes (OLGs) using the dye fura-2. Exposure of OLGs to arachidonic acid (AA) (5-50 microM) elicited a concentration-dependent increase in Cai that was derived mainly from extracellular Ca2+. AA at 50 microM also released Ca2+ from intracellular stores. The response to AA was not decreased by nifedipine or by inhibition of Na(+)-Ca2+ exchange. AA-induced Ca2+ influx pathway was permeable to Mn2+ and Co2+ but not to Ba2+ and was not markedly influenced by depolarization, suggesting that AA activates a voltage-independent, not strictly selective, Ca2+ channel. The Cai response to AA was partially attenuated in the presence of indomethacin, indicating that the Cai response was mediated in part by cyclooxygenase products of AA. However, the AA-induced Cai response far exceeded that induced by prostaglandins and was mimicked by linoleic acid. We conclude that AA modulates Cai of OLGs via two mechanisms: 1) indirectly via cyclooxygenase pathway and 2) directly via membrane lipid-protein interaction.

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