In rats, olfactory bulbectomy (OBX) causes changes in glutamatergic function in the amygdala (AMG) and induces mouse-killing behavior (MKB). The medial AMG (mAMG) plays an important role in the initiation and maintenance of OBX-induced MKB. In the present study, systemic injection or intra-mAMG perfusion of (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine hydrogen maleate (MK-801) was used to determine the effects of MK-801, a noncompetitive N-methyl-d-aspartate (NMDA) receptor antagonist, on the expression of OBX-induced MKB in male Wistar rats that had undergone OBX 1 month previously. The effects of MK-801 on locomotion in OBX rats were also examined using the open-field test. Intraperitoneal injection of MK-801 at doses of 0.10 and 0.15 mg/kg resulted in reversible suppression of MKB, the effect being maximal within 1 h after drug treatment, then gradually disappearing over 6 h. Locomotor distance in OBX rats was not affected using 0.10 mg/kg of MK-801, but increased after treatment with 0.15 mg/kg of MK-801; both doses, however, caused the rats to spend longer in the central area of the open field. MKB was also reversibly suppressed by local perfusion of 1 mM MK-801 at a rate of 1 microl/min into the mAMG through microdialysis probes. These results suggest that NMDA receptors, at least, in the mAMG, are involved in the expression of OBX-induced MKB.