Specific invasion of occipital-to-frontal neocortical grafts by axons from the lateral posterior thalamic nucleus consecutive to neonatal lesion of the rat occipital cortex.

Previous work found that transplants of embryonic (E) day 16 occipital cortex placed into the frontal cortex of newborn hosts failed to receive input from visual-related nuclei of the host thalamus. The present study is aimed at determining the possible causes of the lack of visual-related thalamic input to these transplants. For that purpose, a retrograde neurotracer was injected into transplants of embryonic (E16) occipital origin which were placed into the frontal cortex of newborn rats with either intact or damaged occipital cortex. In rats with intact occipital cortex, occipital-to-frontal transplants were indeed not contacted by axons from the dorsal lateral geniculate (DLG) nucleus and received only sparse to negligible input from, respectively, the lateral posterior (LP) and laterodorsal (LD) thalamic nuclei. Yet, following neonatal lesion of the host occipital cortex, the occipital-to-frontal transplants received a significant input from the LP and to a much lesser degree from the LD but practically none from the DLG. Additional control cases with frontal-to-frontal transplants and prior lesion of the occipital cortex did not receive significant input from any of these thalamic nuclei. Thus, following neonatal deprivation of cortical target cells in their main terminal field, LP and to a lesser extent LD axons have the capacity to recognize and significantly innervate appropriate targets even those at some distance from their normal terminal site. DLG neurons degenerate or are not able to contact and invade available terminal space that is provided at some distance from the occipital cortex.