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Cerebral Cortex 1996; 6:362-376
© Oxford University Press 1996

research-article

Rewiring of Transcortical Projections to Middle Suprasylvian Cortex Following Early Removal of Cat Areas 17 and 18

Margaret A. MacNeil, Stephen G. Lomber and Bertram R. Payne

Department of Anatomy and Neurobiology; Center for Advanced Biomedical Research, Boston University School of Medicine Boston, Massachusetts 02118

Address correspondence to Dr. Margaret A. MacNeil, who is now at Wellman 429, Massachusetts General Hospital, 50 Blossom Street, Boston, MA 02114

reprint requests to Dr. B. R. Payne

Retrograde tracers were injected into middle suprasylvian (MS) cortex of two groups of experimental adult cats that had incurred removal of visual areas 17 and 18 on either the day of birth (P1), or at 1 month of age (P28). Tracers were also injected into the same region of intact and adult ablated control cats. The locations and numbers of labeled neurons in the experimental and control groups were compared. Following lesions on P1, but at no other age, increased numbers of neurons projected to MS cortex. Virtually all of the additional neurons were located in the superficial layers of the ventral posterior suprasylvian (vPS) cortex. These results demonstrated that (1) neurons with ipsilateral transcortical axons have the potential to reconfigure their projections after early, localized cortical damage elsewhere in the cortex of the same hemisphere; (2) this reconfiguration involves expansion of specific projections and is not a generalized capacity of all cortical neurons; (3) the expansion is modality specific; and, finally, (4) the ability of cortical neurons to reorganize projections is limited in time. The expanded projection from vPS to MS cortex may contribute to neuronal compensations and the sparing of visually guided behaviors previously demonstrated in cats with neonatal visual cortex damage, and is a testament to the latent capacities immature cerebral cortical neurons possess to establish new projections following restricted damage to the cerebral cortex early in life.


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