Figure 8. DA receptors modulate ChIs.

A) The I-V curves show current induced by SKF81297 crosses the 0 pA threshold earlier in DAT_dT-2w mice and cAMPS has no effect. For all panels, n=cells. B) The plot shows the zero-crossing point between Na⁺ channel- and SKF81297-dependent inward currents in ChIs from control mice. The intercept between these two excitatory currents lies at a progressively negative voltage in ChIs from C) reserpine and D) DAT_dT-2w mice. E) Quinpirole produces a net inhibitory outward current at potentials close to depolarization. cAMPS blocks this outward current and unmasks a net inhibitory current at hyperpolarized potentials. F) ChI firing in response to applied input current (left) is reduced in ChIs from DAT_dT-2w mice (right). G) The illustration shows that acute-severe DA depletion reduces Chat (dots) and Ihcn to decrease ACh output. DA released from residual boutons weakens ACh release via D2Rs. Moderate-progressive DA deficiency further reduces Ihcn and ACh output; evoked DA release increases ACh efflux via D1Rs. Severe-progressive DA deficiency reduces Chat and Ache and further diminishes Ihcn. See also Figures S5–S8 and Tables S5–S7.