Following focal brain lesions, complex adaptive processes take place in remote intact areas. The present study examines changes in NMDA (N-methyl-D-aspartate), AMPA ((+/-)-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid) and kainate receptors following focal photothrombotic ischemic lesions using quantitative receptor autoradiography. Increases in binding density of NMDA receptors were seen in both hemispheres for up to 30 days. In the contralateral hemisphere, this increase of NMDA receptors occurred as early as 4 h after lesion whereas it appeared with a delay for 14 days on the lesioned side. Binding density of [3H]AMPA and [3H]kainate was unchanged. We suggest that the translational process is differentially regulated by spreading depressions. The delayed up-regulation of NMDA receptor binding on the lesioned side may be due to a translation block similar to that previously described for GABA(A) receptor subunits.