Figure 8.

Inhibiting PKC activation by BiM1 or PKCi_[19-36] prevented D1/D5R-mediated suppression of evoked suprathreshold Ca²⁺ spikes. A, Bath application of the selective PKC inhibitor BiM1 (25 nm) alone did not change the suprathreshold evoked Ca²⁺ spiking properties (peak and area) in PFC neurons. B, D1/D5R activation by DHX (10 μm) in the presence of BiM1 failed to attenuate the Ca²⁺ spike, suggesting that D1/D5R activation attenuates suprathreshold evoked Ca² spikes through PKC activation. C, Subsequent application of a specific L-type Ca² blocker nimodipine (10 μm) suppressed the Ca² spike, whereas further exposure to cadmium (200 μm), a selective blocker of Ca² channels, blocked a residual component of the Ca²⁺ potential so that only the membrane capacitative response remained. Bottom time-compressed traces indicate the time course of the response. D, Using PKCi _[19-36] (10 μm) in the patch pipette did not change the suprathreshold evoked Ca²⁺ spiking properties in PFC neurons. E, D1/D5R activation by DHX (10 μm) with PKCi_[19-36] (10 μm) in the patch pipette failed to attenuate the Ca²⁺ spike, suggesting that D1/D5R activation attenuates suprathreshold evoked Ca² spikes through PKC activation. F, Subsequent application of a specific L-type Ca² blocker nimodipine (10 μm) suppressed the Ca² spike, whereas further exposure to Cd²⁺ (200 μm), a nonselective blocker of all Ca² channels, blocked a residual component of the Ca²⁺ potential so that only the membrane capacitative response remained. Bottom time-compressed traces indicate the time course of the response. G, Histograms of group data showing that D1/D5R activation (DHX alone) suppresses the Ca²⁺ spike, but D1/D5R activation in the presence of a PKC inhibitor (BiM1) or PKCi_[19-36] (10 μm) in the patch pipette prevents the suppression, suggesting that D1/D5R-mediated suppression of suprathreshold evoked Ca²⁺ spikes depends on PKC activation. ^*p < 0.05.