Abstract

The number of callosally projecting neurons (callosal neurons) which can be labeled in cortical areas 17 and 18 by horseradish peroxidase (HRP), injected in the contralateral visual cortex, is reduced to about 50% of normal in cats reared with their eyelids bilaterally sutured. In the same animals the density of HRP anterogradely transported to areas 17 and 18 is also decreased. The apparent loss of callosal neurons is limited to layers III and IV (subzone a), whereas layer VI (subzone c) is unaffected. The effect is obtained after 3 months or more but not after 1 month of deprivation. Two months of visual experience following deprivation do not restitute a normal number of callosal neurons. However, 10 days of normal visual experience preceding the deprivation are sufficient to prevent the effects of the latter. Animals deprived of vision after a short period of normal visual experience and animals allowed normal vision after 1 month of visual deprivation have a more widespread distribution of callosal neurons than do normal animals; in this way they are similar to previously described cats reared with convergent or divergent strabismus, monocular enucleation, or monocular eyelid suture. The results suggest that: vision is actively responsible for both the maintenance and the elimination of fractions of the juvenile callosal connections; the elimination which normally takes place during the second postnatal month requires normal binocular vision; and activity-dependent competition between callosal and other axons can explain the role of vision.

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