Figure 5. DA deficiency reduces Chat, Ache, and Hcn subunit expression.

A) HCN and Na⁺ channel modulation by D1 and D2 receptors. cAMP binds to the HCN CNBD to reduce inhibition of HCN channel gaiting. AC, adenylyl cyclase. B) HA.11 antibody-tagged ChIs from a RiboTag × ChAT-Cre × tdTomato mouse. Bar, 20 μm. C) A single, sharp peak in the melting curve analysis following the RT-qPCR reaction shows that only one product is generated from each primer pair. D) RT-qPCR amplification curves of Chat, Hcn1–4, and Musr18S expressed in ChIs. The number of cycles required to cross C_T is inversely proportional to RNA expression. E_1–4) Relative mRNA expression (2^−ΔC_T) of the Hcn1–4 subunits, where ΔC_T is determined by subtracting C_T from the Musr18S control. DA-deficient mice were processed with their respective controls. For all panels, n=mice. F) Hcn1–4 expression in striata from WT_saline and WT_dT controls, reserpine, and DAT_dT mice. ^&p=0.04, 2-way ANOVA. G₁) Fold-reduction (2^−ΔΔC_T) of mRNA in ChIs from reserpine, G₂) DAT_dT-2w, and G₃) DAT_dT-4w mice relative to their controls. H₁) Charts illustrate changes in the percent distribution of Hcn1–4 subunits based on their gene expression in control, H₂) reserpine, H₃) DAT_dT-2w, and H₄) DAT_dT-4w mice. I) mRNA expression of Chat in ChIs from control mice, and J) Chat, K) Ache, and L) Vachat relative to their controls. See also Table S4.