In contrast, activation of dopamine D2 receptors causes a long-term depression (LTD) of the DA-dependent slow IPSC 116. This LTD is inhibited by the presence of the calcium chelator BAPTA in the recordings pipette, and seems therefore to rely on a cell-autonomous postsynaptic effect (Figure 3A). This reduction in inhibition would be expected to increase burst firing and DA release in the terminal projections in vivo. Less is known concerning the mechanism of this plasticity but could involve desensitization of D2 receptors, modulation of G-protein function and/or GIRK channel availability (as GIRK channels can rapidly redistribute).
