Polyunsaturated fatty acids (PUFA), have been implicated in the modulation of a variety of biochemical processes in the cells. They were able to interact with the membrane proteins including ion channels in normal and pathological conditions. The aim of the project was to determine whether the neuroprotective mechanism of the large-conductance calcium-activated potassium (mitoBKCa) channel from the inner mitochondrial membrane can be explained by mutual interaction between the channels and polyunsaturated fatty acids. The study was performed using patch-clamp technique and mitochondria isolated from rat astrocytes. We analyzed effect of arachidonic acid (AA), eicosatetraynoic acid (ETYA) a non-metabolizable analog of AA, docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA). The open probability of the channel did not change significantly after application of 10 μM ETYA, but after adding 10 μM AA open probability increased. This suggest that channel is affected by metabolites of AA rather than fatty acids itself. Application of 30 μM DHA, and 30 μM EPA increased open probability of the channel. Also number of the open channels in the patch increased in the presence of 30 μM EPA. Summarising, our results indicate that neuroprotective PUFAs, like DHA and EPA activate mitoBKCa channel, while proapoptotic and proinflamatory AA had no effect on mitoBKCa channel. Grant support DEC-2011/01/N/NZ1/04311
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