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This Article Full Text Full Text (PDF) All Versions of this Article: 99/5/2086    most recent 00871.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by McManus, J. N. J. Articles by Gilbert, C. D. PubMed PubMed Citation Articles by McManus, J. N. J. Articles by Gilbert, C. D.

A Computational Model of Perceptual Fill-in Following Retinal Degeneration

¹Rockefeller University, New York, New York; and ²Department of Computer Science and Applied Mathematics, The Weizmann Institute, Rehovot, Israel

Submitted 6 August 2007; accepted in final form 15 January 2008

The ablation of afferent input results in the reorganization of sensory and motor cortices. In the primary visual cortex (V1), binocular retinal lesions deprive a corresponding cortical region [lesion projection zone (LPZ)] of visual input. Nevertheless, neurons in the LPZ regain responsiveness by shifting their receptive fields (RFs) outside the retinal lesions; this re-emergence of neural activity is paralleled by the perceptual completion of disrupted visual input in human subjects with retinal damage. To determine whether V1 reorganization can account for perceptual fill-in, we developed a neural network model that simulates the cortical remapping in V1. The model shows that RF shifts mediated by the plexus of spatial- and orientation-dependent horizontal connections in V1 can engender filling-in that is both robust and consistent with psychophysical reports of perceptual completion. Our model suggests that V1 reorganization may underlie perceptual fill-in, and it predicts spatial relationships between the original and remapped RFs that can be tested experimentally. More generally, it provides a general explanation for adaptive functional changes following CNS lesions, based on the recruitment of existing cortical connections that are involved in normal integrative mechanisms.