Arachidonic acid inhibits potassium conductances in cultured rat
oligodendrocytes.
Soliven, Betty, and Ning Wang.
Department of Neurology,The Brain Research Institute, The
University of Chicago, Chicago, IL 60637
APStracts 2:0089C, 1995.
Arachidonic acid (AA) and its metabolites play a dual role as
intracellular second messengers and as transcellular mediators of
neural activity. We have previous shown that AA increases cytosolic
Ca2+ in oligodendrocytes (OLGs). In this work, we studied the effects
of arachidonic acid and other fatty acids on whole-cell K+ currents
of cultured rat OLGs using the patch-clamp technique. We found that:
1) arachidonic acid 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 signalling
in OLGs, that is, 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 OLGs.
Received 2 December 1994; accepted in final form 13 January 1995.
APS Manuscript Number C703-4.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 28 February 1995.