Phosphodiesterase-10A inverse changes in striatopallidal and striatoentopeduncular pathways of a transgenic mouse model of DYT1 dystonia
In most forms of dystonia, brain regions have functional rather than structural abnormalities. We report that changes of phosphodiesterase-10A (PDE10A) can map functional imbalance of basal ganglia circuits in a mouse model of DYT1 dystonia overexpressing mutant torsinA. PDE10A is a key enzyme in the catabolism of second messenger cAMP/cGMP, whose synthesis is stimulated by D1 or inhibited by D2 receptors, expressed in striatoentopeducuncular or striatopallidal pathways respectively. PDE10A was studied in control mice and in mice carrying either human wild-type torsinA or mutant torsinA.