EN
Glutamatergic dysfunction has been implicated in psychiatric disorders such as schizophrenia. Stimulation of the metabotropic glutamate (mGlu) 2/3 receptor have been shown to be effective in a number of animal models of schizophrenia. For modelling symptoms of schizophrenia a selective and non-competitive NMDA receptor antagonist MK801 were used. The administration of MK801 evoked hyperactive locomotor behavior with increases in distance travelled, speed, and clockwise/anticlockwise locomotion, and a marked decrease in rearing behavior and disruption of PPI in mice. The intraperitoneal administration of a positive modulator mGlu2-receptor Biphenylindanone A (BINA) reversed disrupted PPI evoked by MK801 administration and improve locomotion impairment. These findings indicate that the stimulation of the mGlu2 receptor improved locomotion impairment elicited by MK-801, and such manipulations could be effective approaches for the treatment of behavioral dysfunctions observed in schizophrenic patients.