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Arachidonic Acid and Other Unsaturated Fatty Acids Alter Membrane Potential in PC12 and Bovine Adrenal Chromaffin Cells
Author(s) -
Ehrengruber M. U.,
Deranleau D. A.,
Kempf C.,
Zahler P.,
Lanzrein M.
Publication year - 1993
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1993.tb05849.x
Subject(s) - hyperpolarization (physics) , valinomycin , arachidonic acid , chromaffin cell , membrane potential , fatty acid , biochemistry , chemistry , ionophore , biophysics , tetraethylammonium , depolarization , unsaturated fatty acid , membrane , biology , endocrinology , potassium , stereochemistry , adrenal medulla , organic chemistry , catecholamine , nuclear magnetic resonance spectroscopy , enzyme
The action of arachidonic acid and other fatty acids on membrane potential in PC 12 and bovine chromaffin cells was investigated using a membrane potential‐sensitive fluorescent dye. Arachidonic acid (1–40 μ M ) provoked dose‐dependent membrane hyperpolarization, thereby reducing hyperpolarization induced by the K + ‐selective ionophore valinomycin. Other cis‐unsaturated fatty acids, but not lipoxygenase products or the saturated fatty acid palmitic acid, also affected membrane potential. Tetraethylammonium blocked the arachidonic acid‐induced hyperpolarization. These data suggest that cis‐unsaturated fatty acids alter membrane potential in PC 12 and bovine chromaffin cells by modulating K + conductances. Valinomycin‐generated hyperpolarization had no effect on agonist‐induced Ca 2+ influx into bovine chromaffin cells, whereas preincubation with arachidonic acid and other cis‐unsaturated fatty acids blocked Ca 2+ influx and secretion. We propose a model where internally generated fatty acids act as a feed‐back to desensitize the stimulated cell via inhibition of receptor‐dependent Ca 2+ influx and induction of membrane hyperpolarization.

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