Modulation of a variety of voltage-dependent potassium channels by arachidonic acid has been well documented [Meves, 94]. Despite multiple hypotheses suggested and a lot of experimental work done, there is still uncertainty which of the hypothetic mechanisms of A-type current accounts for modulation by fatty acids. Given the central importance of voltage-gated potassium channels in neuronal excitability it is not surprising that probably several mechanisms contribute to their tight control. This study was designed to investigate whether oxidative processes also contribute to AA-induced modulation of I_A. In order to test this hypothesis, some specific goals had to be defined:

• What is the effect of AA in hippocampal neurons from acute brain slices?

• Is this effect direct or an effect of one or more of its multiple metabolites?

• How does AA affect neurons in different areas of the hippocampus?

• Are there differences in A-type channels in untreated stellate cells and pyramidal neurons of the entorhinal cortex?

• Do A-type currents respond differently to 1 pM AA in neurons of the CA1 and neurons of the entorhinal cortex?

• Is oxidation involved in AA effects?

• Is it possible to identify the molecular basis of these effects, and the involved subunits?