Neonatal superior collicular lesions alter visual callosal development in hamster.

Visual callosal connections were examined using autoradiographic (ARG) and horseradish peroxidase (HRP) techniques in normal adult hamsters, and in adults subjected to ablation of the superficial tectal laminae at birth. Additional ARG and HRP experiments were carried out in hamsters 1-27 days of age in order to describe the normal development of this pathway. Neonatal collicular lesions, which deprived visual cortical neurons of a major terminal zone in the midbrain, substantially altered the visual callosal pathway. In the lesioned animals, the numbers of supragranular callosal cells in the 17-18a border region and lamina VI callosal neurons in medial area 17 were significantly greater than normal. The ARG experiments demonstrated additional clearcut abnormalities in the visual callosal pathway of the lesioned hamsters. First, the mediolateral extent of the supragranular callosal zone around the 17-18a border was increased. Secondly, dense label was visible over lower layer V and lamina VI throughout area 17. Finally, labelling in lamina I could also be observed across the entire mediolateral extent of area 17. Experiments in the developing hamsters suggested that some of the abnormalities observed in the lesioned animals may have resulted from the maintenance of normally transient developmental states. During the first postnatal week, both callosal cells and anterograde labelling were evenly distributed throughout the dorsal posterior neocortex, but only in the subplate region. During the second postnatal week, supragranular callosal cells were also labelled in both medial and lateral area 17, but from their first appearance, they were always most numerous in the 17-18a border region. At the same time callosal axons invaded the supragranular laminae, but only near the 17-18a border. By the end of the second postnatal week, the visual callosal pathway was very similar to that in the adult.