Brain hyperexcitability has been proposed to a cause series of neuropsychiatric disorders. It is controlled by neurons and astrocytes. In astrocytes, the glial glutamate transporters GLT1 and GLAST are responsible for regulating brain excitability. However, the role of glial glutamate transporters in the pathogenesis of neuropsychiatric disorders remains unknown. We show that GLT1 inducible knockout (GLAST^CreERT2/+/GLT1^flox/flox, iKO) mice developed severe facial skin lesions and exhibited pathologic repetitive behaviour such as self-grooming. Although the repetitive behaviour is the common core symptoms of autism, obsessive compulsive disorder (OCD) and Tourette's syndrome, iKO mice did not exhibit other autism- or OCD-like symptoms (anxiety and abnormal social behaviour), but rather exhibited other Tourette's syndrome-like tics. Seizure sensitivity and excitatory transmission at the corticostriatal synapses after repetitive stimulation were increased in iKO mice. Furthermore, administration of an N-methyl-D-aspartate (NMDA) receptor antagonist memantine suppressed the pathologic repetitive behaviours in iKO mice. These data suggest that iKO mice as a novel animal model for Tourette's syndrome and suppression of brain hyperexcitability by NMDA receptor blockade may be effective for Tourette's syndrome.