Suppression of neuronal potassium A-current by arachidonic acid.
The effect of arachidonic acid on the A current (IA) has been studied in dissociated bullfrog neurons under whole-cell voltage-clamp conditions. Arachidonic acid reduced IA in a dose-dependent and reversible manner without a shift in the prepulse inactivation voltage-current relation. 1.75 microM inhibited IA by 50%, and higher concentrations caused a total suppression. In addition, arachidonic acid increased the M-current (IM), a different potassium current that does not inactivate. Neither indomethacin nor nordihydroguaiaretic acid, cyclooxygenase and lipoxygenase inhibitors respectively, prevented IA reduction. In contrast, nordihydroguaiaretic acid prevented IM enhancement. Eicosatetraynoic acid, an arachidonic acid analog that cannot be metabolized, also reduced IA. These results suggest that arachidonic acid metabolism is not required to suppress IA.
Villarroel
A
A
Howard Hughes Medical Institute, Department of Neurobiology and Behavior, SUNY at Stony Brook 11794-5230.
D000818:Animals; D016718:Arachidonic Acid / Q000502:physiology*; D066298:In Vitro Techniques; D007213:Indomethacin / Q000494:pharmacology; D009637:Masoprocol / Q000494:pharmacology; D008564:Membrane Potentials / Q000502:physiology; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D015221:Potassium Channels / Q000187:drug effects / Q000502:physiology*; D011892:Rana catesbeiana
D015221:Potassium Channels; D016718:Arachidonic Acid; D009637:Masoprocol; D007213:Indomethacin