Tourette Syndrome (TS) is a neurodevelopmental disorder characterized by motor and vocal tics arising from altered corticostriatal function. Along with tics, individuals often experience premonitory urges and compulsive/habit-like tendencies. These behaviors overlap with comorbidities like obsessive-compulsive disorder, autism spectrum disorder, and attention-deficit hyperactivity disorder - suggesting shared cognitive changes to action learning and control. The behavioral and genetic complexity of TS presents difficulty in developing translational animal models. To address this challenge, our lab generated transgenic mouse models harboring de novo human mutations in the high-confidence TS risk gene, Celsr3. This talk will discuss our use of behavioral assays and in vivo neural recordings to characterize how Celsr3 mutations alter action learning and suppression. Our results reveal accelerated motor learning and behavioral inflexibility linked to changes in striatal dopamine. These findings suggest a mechanistic basis for how tics may be learned and can inform more precise intervention strategies for TS.