The distribution of corticopontine projections was studied, primarily with the Fink-Heimer technique, in adult rats which at 2-3 days of age had sustained unilateral sensorimotor (SMC) or occipital (OC) cortical lesions and in animal that had received neonatal hemocerebellar (HCb) lesions singly or in combination with the neonatal SMC or OC lesions. Neonatal left SMC or left HCb lesions induced an anomalous increase in crossed sensorimotor corticopontine (SMP) projections originating from the right SMC. This increase appeared more dense after cortical lesions as compared to cerebellar lesions and appeared more dense in those animals receiving the combined SMC plus HCb lesions. No alterations in the distribution of SMP fibers were observed after neonatal OC lesions nor were any alterations of occipital corticopontine (OP) fibers observed in any of the neonatal lesion groups. The remodelling of right SMP projections after neonatal left SMC lesions demonstrates an interaction between corresponding pathways originating from opposite sides of the brain and which occurs in response to the partial removal of afferents to pontine gray neurons as a result of the SMC lesions. In contrast, the absence of SMP plasticity after OC lesions, and vice versa, demonstrates the absence of plasticity between pathways which differ anatomically and functionally. The substantial neuronal loss which occurs within the right PG after neonatal left HCb lesions is believed to influence the increase in crossed SMP fibers coursing from the right hemisphere to the larger left PG. No increase in crossed OP fibers from the right hemisphere was observed in these animals. The increase in crossed SMP fibers after neonatal SMC lesions combined with neonatal HCb lesions is more dense than found in the single lesion groups. These findings suggest that separate mechanisms of plasticity might be operational for each lesion and that these mechanisms may be additive.