Restoration of brightness discrimination was studied in adult rats after controlled crush of the optic nerve in order to further characterize a recently introduced experimental brain injury model. Mild, moderate or severe crush of the optic nerve produced partial or complete loss of the ability to perform a brightness discrimination task. Two to three weeks following mild injury we observed nearly complete spontaneous behavioural recovery whereas recovery was more limited after moderate and totally absent after severe crush. Horseradish peroxidase (HRP) injected into the superior colliculus was transported retrogradely across the lesion site and accumulated in retinal ganglion cells (RGCs). Two days following mild, moderate or severe crush, 28, 23 and 8% respectively of RGCs were found to be labelled with HRP, indicating that they are still connected with their target and are therefore presumably intact. RGC loss affected all areas of the retina homogeneously. At postoperative day 14, the number of morphologically 'intact' RGCs declined even further to 11% in the mild injury group, despite our observation of recovery of vision to near-normal levels. The mechanism whereby such impressive neuronal plasticity is achieved despite the rather small number of intact RGCs is still unknown. However, further studies of the crush model using additional behavioural, morphological and electrophysiological techniques may allow us to determine more clearly the biological basis of recovery of function after central nervous system injury.