Modulation of calcium-activated potassium small conductance (SK) current in rat dopamine neurons of the ventral tegmental area.

Block of calcium-sensitive potassium SK current (gKCa([SK])) by apamin or bicuculline methiodide potentiates burst firing in dopamine neurons in the presence of N-methyl-D-aspartate (NMDA). The purpose of this study was to test the hypothesis that calcium entry through NMDA-gated channels can potentiate gKCa([SK]) in dopamine neurons in the ventral tegmental area. We used microelectrodes to record an outward tail current that was evoked by membrane depolarization under single-electrode voltage-clamp. Using bicuculline methiodide (50 microM) as a reversible inhibitor of gKCa([SK]), we found that NMDA (15 microM) reduced the peak amplitude of the outward tail current by 39%. Contrary to expectations, our results suggest that stimulation of NMDA receptors reduces the calcium-activated potassium gKCa([SK]), an effect that could facilitate NMDA-dependent burst firing.