In Syrian hamsters, mature retinal terminals contain only low levels of the growth-associated protein, GAP-43, whereas the lateral posterior nucleus (LP) of the thalamus contains high levels of this protein. Damage to the superior colliculus in neonatal hamsters induces retinal terminals to form dense patches of innervation in the LP, an area which otherwise receives little if any direct retinal input. The present study used GAP-43 antibodies to examine the interaction between abnormally routed optic fibers and the cells in the anomalous thalamic target zone. Immunohistochemistry revealed very little GAP-43 in the abnormal retinal projection to the LP, indicating that the normal developmental decline in GAP-43 levels occurs even in an inappropriate extracellular environment. Moreover, retinal fibers were found to exclude the protein from its normal territory, forming negatively-stained islands in those regions of the LP containing the retinal terminals. In order to identify the normal source of GAP-43-positive terminals in the LP, we surgically removed two major extrinsic afferents to this region, or we chemically eliminated local interneurons. Whereas removing projections from the SC or posterior cortex did not alter GAP-43 immunoreactivity in the LP, destruction of local interneurons with ibotenic acid resulted in markedly diminished levels of this protein. These results show that retinal terminals induced to form in an abnormal target area undergo their normal diminution of GAP-43, and that these retinal projections displace other GAP-43-rich terminals in the LP that appear to arise from local interneurons.