Intracellular arachidonic acid potently reduces the transient K-current IA in rat hippocampal neurons via an oxidative mechanism.
May modulate excitability in rodent neurons; leaves open in vivo relevance or human translation.
Membrane-permeable arachidonic acid (AA) is liberated in a Ca2+-dependent way inside cells. By using whole cell patch clamp we show that intracellular AA (1 pM) selectively reduces IA in rat hippocampal neurons, whereas extracellular application requires a 10(6)-fold concentration. The nonmetabolized AA analogue ETYA mimics the effect of AA that is blocked by ascorbic acid or intracellular glutathione, suggesting an intracellular oxidative mechanism. We conclude that intracellular AA is extremely potent in reducing IA by an oxidative mechanism, particularly during oxidative stress.
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Bittner et al. (1999) studied this question.
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