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AJP - Cell Physiology, Vol 269, Issue 2 C341-C348, Copyright © 1995 by American Physiological Society
ARTICLES |
B. Soliven and N. Wang
Department of Neurology, University of Chicago, Illinois 60637, USA.
Arachidonic acid (AA) and its metabolites play a dual role as intracellular second messengers and as transcellular mediators of neural activity. We have previously shown that AA increases cytosolic Ca2+ in oligodendrocytes. In this work, we studied the effects of AA and other fatty acids on whole cell K+ currents of cultured rat oligodendrocytes using the patch-clamp technique. We found that 1) AA decreased the current amplitudes of both the inwardly rectifying K+ current (IKir) and the outward K+ currents (IKo) resulting in membrane depolarization; 2) AA also induced IKo current inactivation/blocked state; 3) AA appeared to act directly on K+ channels and not indirectly via its metabolic products, activation of protein kinase C, or by generation of oxygen free radicals. We have thus demonstrated an additional mechanism for AA-induced signaling in oligodendrocytes, i.e., via modulation of K+ conductances leading to membrane depolarization. The latter has been shown to influence protein phosphorylation and perhaps other important functional output of oligodendrocytes.
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H. Hida, M. Takeda, and B. Soliven Ceramide Inhibits Inwardly Rectifying K+ Currents via a Ras- and Raf-1-Dependent Pathway in Cultured Oligodendrocytes J. Neurosci., November 1, 1998; 18(21): 8712 - 8719. [Abstract] [Full Text] [PDF] |
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B. Attali, N. Wang, A. Kolot, A. Sobko, V. Cherepanov, and B. Soliven Characterization of Delayed Rectifier Kv Channels in Oligodendrocytes and Progenitor Cells J. Neurosci., November 1, 1997; 17(21): 8234 - 8245. [Abstract] [Full Text] [PDF] |
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