Presynaptic modulation by dopamine and GABA opens a potassium channel in rat cortical, striatal and hippocampal synaptosomes via eicosanoids.

Using a K(+)-sensitive electrode in synaptosomal preparations, the presynaptic modulating effect of dopamine and GABA in opening a K+ channel was investigated. In cortical, striatal and hippocampal synaptosomes dopamine D1 and D2 agonists and a GABAB agonist promoted the efflux of K+ in all three preparations. The effect was blocked by the cyclooxygenase inhibitor, indomethacin suggesting that eicosanoids act as second messengers in these systems. The inference in these studies is that dopamine and GABA hyperpolarize presynaptic terminals thereby reducing Ca2+ influx and thus inhibiting the evoked release of transmitters.