Figure 6.

Buspirone prevents PACAP and VIP neuropeptide dysregulations in the brain of rotenone-treated mice. Real-time qPCR analyses of PACAP and VIP mRNA expression in the midbrain (A,B), striatum (F,G), prefrontal cortex (K,L), amygdala (P,Q), and hippocampus (U,V) following the administration of rotenone (10 mg/kg) and/or buspirone (1, 3, or 10 mg) daily for 21 days. Fold-changes were calculated using the ΔΔCt method after normalization to s18 (ribosomal protein s18 gene), the housekeeping gene. Each data point represents the mean value from n = 5–8 mice per each group. Representative Western blots and densitometry of PACAP and VIP protein expression in the midbrain (C–E), striatum (H–J), prefrontal cortex (M–O), amygdala (R–T), and hippocampus (W–Y). Protein expression was normalized to GAPDH, the loading control. Western blots are cropped and removed lanes depicting drug-treatment controls are included in Supplementary Figure S6. Densitometric results are expressed as means ± S.E.M from n = 5–8 mice per each group. * p < 0.05, ** p < 0.01, *** p < 0.001, or **** p < 0.0001, compared to vehicle-treated controls; or # p < 0.05, ## p < 0.01, ### p < 0.001, or #### p < 0.0001, compared to rotenone (10 mg/kg)-treated mice, as determined by an ANOVA followed by Sidak’s post-hoc test. PACAP, pituitary adenylate cyclase-activating peptide; VIP, vasoactive intestinal peptide; s18, ribosomal protein s18 gene; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; kDa, Kilodalton.