We investigated in the striate cortex of kittens whether the recovery from the effects of monocular deprivation that occurs after reverse occlusion requires activation of N-methyl-D-aspartate (NMDA) receptors. The right eye of 3-4-week-old kittens was closed by lid suture for one week. Subsequently this eye was reopened and the left eyelid sutured closed for another week. During this second week, the NMDA-receptor antagonist, 2-amino-5-phosphonovaleric acid (APV), was infused from an osmotic minipump into the left visual cortex (50 nmol/h), while the right visual cortex was infused only with vehicle solution (saline) as control. At the end of the second week, the ocular dominance of striate cortical neurons was assessed with single unit recording. In the control hemispheres, the large majority of neurons was dominated by the newly opened eye, while in the APV-treated hemispheres most neurons were still dominated by the newly deprived eye. In addition, neurons in the APV-treated hemispheres were less responsive and showed a reduction of orientation tuning. These data confirm that chronic blockade of cortical NMDA-receptors disrupts the disconnection of deprived pathways after monocular deprivation and reduces both responsiveness and orientation selectivity of cortical neurons. In addition they indicate that blockade of NMDA-receptors prevents also vision-dependent recovery of deprived pathways after reverse occlusion.