Figure 6.

Modulation of IRKC by upstream components of the cAMP–PKA pathway. Perfusion of Sp-cAMP (100 μm) inhibits IRKC amplitude in some neurons (A) but enhances it in others (B). C, A summary shows that modulation of IRKC by D₁R signaling diverges at the level of cAMP. When D₁R was stimulated with a relatively higher intensity (5 μm SKF81297), the IRKC amplitude was suppressed >15% in 14 of 28 recorded neurons, whereas 4 of 28 recorded neurons displayed enhanced IRKC (enhancement, >15%), and the additional 10 neurons did not display obvious alterations (changes within 15%). Similar responses were observed when the neurons were perfused with the partial D₁R agonist SKF 38393 (5 μm). IRKC was suppressed >15% in 7 of 20 neurons, whereas in 5 of 20 recorded neurons, exhibited enhanced IRKC (>15%). No obvious alterations (change, <15%) were observed in the other eight neurons. Perfusion of forskolin (20 μm) induced similar divergent modulation of IRKC, suppression (>15%) in 6 of 15 recorded neurons, enhancement (>15%) in 4 of 15 neurons, and no obvious alterations (change, <15%) in the other five neurons. Perfusion of 100 μm Sp-cAMP also induces divergent modulation of IRKC: suppression (15%) in 5 of 14 neurons, enhancement (>15%) in 5 of 14 neurons, and no obvious alterations (change, <15%) in the other four neurons. Cnl, Control; Wash, washout.