DEVELOPMENT OF ABNORMAL LAMINATION AND BINOCULAR SEGREGATION IN THE RETINOTECTAL PATHWAYS OF THE RAT

The uncrossed retinotectal pathway of pigmented rats originates from a small fraction of the retinal ganglion cell population. This projecti on terminates deeply in discrete patches within the upper grey layers where crossed and uncrossed inputs overlap. However, after the experim ental enlargement of the uncrossed pathway, the ipsilateral fibers are also found in a superficial tier of the upper grey layers where binoc ular inputs segregate [36]. We studied the development of the retinote ctal projections in rats after the enlargement of the uncrossed pathwa y as a result of a contralateral (left) optic tract lesion (OTL) made at birth. Horseradish peroxidase (HRP) was used as an anterograde trac er. An abnormal uncrossed projection from the Light Rye to the collicu lar surface appeared at postnatal day 3 (P3). Between P5 and P10, this projection developed the bilaminar pattern seen in similarly operated adults. The laminar arrangement of the aberrant terminal fields did n ot change significantly after an ipsilateral visual cortex ablation on the day of birth. Despite the early development of the aberrant uncro ssed pathway, binocular segregation was incipient at P10. At P14, 46% of the operated rats presented gaps in the terminal labeling at the te ctal surface. This figure increased to 55.5% at 6 weeks, a proportion still smaller than in adult animals of the same group (69%). Eyelid su ture had no effect on segregation. This projection remains plastic for at least 3 weeks, since the removal of the ipsilateral input at eithe r P14 or P21 resulted in the absence of gaps in the contralateral proj ection. We conclude that the laminar selection of retinotectal project ions depends on binocular interactions and that the abnormal segregati on of retinal inputs to the superior colliculus has an unusually protr acted development which can be reversed long after the previously defi ned critical period in this system.