Recent developments in the neurobiology of anxiety have highlighted the neurotransmitter glutamate as an important element in anxiety-related behavior. Particularly, experimental evidences that support roles for glutamatergic synapses within the striatum in mood disorders are increasing. The striatum receives convergent excitatory inputs from the cortex and the thalamus and forms the efferent connection to the basal ganglia through the direct (striatonigral) and indirect (striatopallidal) pathways, which are involved in motor and cognitive function control. Because the basal ganglia provides input to the thalamus, and this input is modulated by the balance between the direct and indirect pathways, the regulation of corticostriatal synapses through which the striatum receives major excitatory input seems to be critical for maintaining this balance. Here we examined the effect of altering glutamatergic synapses in the striatum of mice within the context of anxiety-related behavior. Mice that express the G2CT peptide, which interferes with AMPAR trafficking, specifically in the striatum show increased anxious behaviors in the several anxiety-related behavioral tests. Our results suggest that the alteration of glutamatergic synapses, especially the synaptic strength and structure in the striatum can affect anxiety-related behavior and that the tilted balance between the direct pathway and the indirect pathway may underlie these behavioral abnormalities.