Amplification of Thalamic Projections to Middle Suprasylvian Cortex following Ablation of Immature Primary Visual Cortex in the Cat

Abstract

The purpose of the present study was to identify expansions in thalamic projections to the middle suprasylvian (MS) cortex that could be linked to the sparing of visually guided behaviors that follow the removal of visual cortex early in postnatal life. Injections of retrograde tracers were made into the medial bank of the middle suprasylvian sulcus in intact, adult cats and in adult cats that had incurred ablations of areas 17 and 18 on the day of birth (P1), P28, or ≥6 months of age, and the numbers of labeled neurons in the thalamus were counted. In the thalamus of the intact cat, the greatest number of labeled neurons are located in the lateral divison of the lateral posterior nucleus and there are intermediate numbers in the medial division of the lateral posterior nucleus (LPm); and smaller numbers within the medial interlaminar nucleus, the C-complex of the dorsal lateral geniculate nucleus (dLGN), the geniculate wing, and the pulvinar nucleus. Following the removal of areas 17 and 18 at different ages, thalamic projections to MS cortex exhibit an age-dependent reorganization. Removals on P1, induce twice the normal number of neurons in LPm and three times the normal number of neurons in the C-complex of dLGN to project to MS cortex. Removals on P28 induce five times the normal number of neurons in the C-complex to project to MS cortex. In addition, removals at both ages resulted in projections from the A-laminae to MS cortex becoming permanently established. No changes in the pattern or number of neurons that project to MS cortex were detected when areas 17 and 18 were removed in adulthood. These results show that pathways through the C-complex of dLGN and through LPm expand substantially following ablation of immature areas 17 and 18. These expanded pathways are linked to Y- and W-functional streams of visual signals that are relayed from the retina to extrastriate cortex either directly through dLGN or indirectly via the superior colliculus and LPm. These signals may be critical for the sparing of neural operations following ablation of areas 17 and 18 early in development.