The disclosure describes a unique animal model which is useful for studying the role of FGF14 in the central nervous system (CNS) and testing of potential drugs for treatment of CNS diseases. To provide this animal model, the Fgf14 gene is disrupted in mice by replacing the second and third exons with beta-galactosidase. Neuropharmacological studies are disclosed which show that the Fgf14 deficient mice have disrupted striatal-nigra and striatal-pallidal pathways resulting in increased excitatory input to the cortex. The paroxysmal hyperkinetic disorder in Fgf14 deficient mice phenocopies a form of dystonia, a disease often associated with dysfunction of the putamen.
