Abstract The capacity for structural and functional remodeling in damaged adult CNS sensory systems can be studied by replacement of neurons in damaged structures by fetal cells from these anatomical origins. For integration to take place, the replacement paradigm assumes that (a) reconnection of adult host afferent fibers onto developing neurons is possible and (b) that the correct molecular signals exist also in the adult brain for fetal neurons to extend axons and pattern synaptic contacts. We have tried to answer some of these fundamental questions by using neuronal depletion models followed by neuronal replacement in the adult rat CNS (Isacson et al. 1984. Nature (London) 311: 458–460; Isacson et al. 1988. Prog. Brain Res. 78: 13–27; Nothias et al. 1988. Brain Res. 461: 349–354; Peschanski and Isacson. 1988. J. Comp. Neurol. 274: 449–463; Sofroniew et al. 1990. Prog. Brain Res. 82: 313–320). In one such model, kainic acid infusions deplete the ventrobasal complex (VB) of all neurons projecting to the somatosensory cortex, while afferent axons from the lemniscal and monoaminergic systems remain in the area. Direct implantation of fetal neurons (gestation age 15–16) of ventrobasal destination allows reconnection of circuitry to take place at the thalamic level, as studied by anatomical tracers, electron microscopy, and functional 2-deoxyglucose studies, while fetal thalamic VB neurons appear less likely to growt through the internal capsule toward the cortical level.