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 projection terminates deeply in discrete patches within the upper grey layers where crossed and uncrossed inputs overlap. However, after the experimental enlargement of the uncrossed pathway, the ipsilateral fibers are also found in a superficial tier of the upper grey layers where binocular inputs segregate [36]. We studied the development of the retinotectal projections in rats after the enlargement of the uncrossed pathway as a result of a contralateral (left) optic tract lesion (OTL) made at birth. Horseradish peroxidase (HRP) was used as an anterograde tracer. An abnormal uncrossed projection from the right eye to the collicular surface appeared at postnatal day 3 (P3). Between P5 and P10, this projection developed the bilaminar pattern seen in similar operated adults. The laminar arrangement of the aberrant terminal fields did not change significantly after an ipsilateral visual cortex ablation on the day of birth. Despite the early development of the aberrant uncrossed pathway, binocular segregation was incipient at P10. At P14, 46% of the operated rats presented gaps in the terminal labeling at the tectal surface. This figure increased to 55.5% at 6 weeks, a proportion still smaller than in adult animals of the same group (69%). Eyelid suture had no effect on segregation. This projection remains plastic for at least 3 weeks, since the removal of the ipsilateral input at either P14 or P21 resulted in the absence of gaps in the contralateral projection. We conclude that the laminar selection of retinotectal projections depends on binocular interactions and that the abnormal segregation of retinal inputs to the superior colliculus has an unusually protracted development which can be reversed long after the previously defined critical period in this system.
Serfaty
C A
CA
Instituto de Biofísica, Universidade Federal do Rio de Janeiro, Brazil.
Linden
R
R
D000375:Aging / Q000502:physiology*; D000818:Animals; D001370:Axonal Transport; D001766:Blindness; D002540:Cerebral Cortex / Q000502:physiology*; D015353:Eye Enucleation; D005143:Eyelids; D006735:Horseradish Peroxidase; D051381:Rats; D011919:Rats, Inbred Strains; D012016:Reference Values; D012160:Retina / Q000254:growth & development; D012165:Retinal Ganglion Cells / Q000166:cytology / Q000502:physiology; D013477:Superior Colliculi / Q000033:anatomy & histology* / Q000254:growth & development / Q000502:physiology; D015348:Vision, Binocular; D015349:Vision, Monocular; D014795:Visual Pathways / Q000033:anatomy & histology* / Q000254:growth & development / Q000502:physiology
D006735:Horseradish Peroxidase