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Development of ocular dominance columns in the absence of retinal input

Abstract

The initial establishment of ocular dominance columns in visual cortex is believed to involve the segregation of overlapping geniculocortical axons into eye-specific patches based on patterns of correlated activity. However, we found that total removal of retinal influence early in visual development did not prevent segregation of geniculocortical axons into alternating stripes with periodicity normal for ocular dominance columns. Because the patterning of geniculocortical afferents resists this dramatic change in the level, source and pattern of spontaneous activity, we propose that formation of ocular dominance columns relies on molecular cues present on thalamic axons, cortical cells or both.

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Figure 1: Focal biotinylated dextran amine (BDA) injections in LGN reveal segregated geniculocortical afferents in striate cortex of normal and enucleated animals.
Figure 2: Anterogradely labeled patches in enucleates have the same spacing as normal ocular dominance columns.
Figure 3: Segregated geniculocortical axons in enucleates form ocular dominance-like stripe patterns.
Figure 4: Retrograde label of LGN by microinjections of fluorescent microspheres in visual cortex demonstrates normal topography and eye-specific termination patterns of geniculocortical axons.

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Acknowledgements

We thank David Fitzpatrick, Richard Mooney, Michael Weliky and Hadley Wilson Horch for their insightful comments and Barbara Chapman for conveying unpublished research on the ferret ocular dominance critical period. Megan Gray, Stuart Portbury and Scott Douglas provided technical assistance. This work was supported by the NIH (NEI EYO7960, L.C.K.) and predoctoral fellowships to J.C.C. from the Ruth K. Broad Biomedical Research Foundation and the NIH (NIMH, NRSA MH12359).

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Correspondence to Justin C. Crowley.

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Crowley, J., Katz, L. Development of ocular dominance columns in the absence of retinal input. Nat Neurosci 2, 1125–1130 (1999). https://doi.org/10.1038/16051

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