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Notes: Summary Visual callosal connections were examined using the horseradish peroxidase (HRP) technique in normal, neonatal and adult C57BL mice, and in adults of this strain which were bilaterally enucleated within 12 h of birth. In addition, callosal connections were also delineated in two strains of congenitally anophthalmic mice, ZRDCTan and orJ. Material from 129/J mice served as controls for the latter strain. In normal adults anterograde labelling and HRP labelled cells were visible primarily at the borders of area 17. In the 17–18a border region, labelled neurons were located primarily in layers II–III and V. In the medial striate cortex, a small number of labelled cells were present, primarily in lamina VI. Anterograde HRP labelling in the normal adults was also located primarily at the borders of area 17. At the 17–18a border, it was very heavy in layers V and VI, somewhat lighter in layer IV, and fairly dense in layers II–III and the lower half of lamina I. Labelling indicative of anterograde HRP transport was also visible in lowermost lamina V and layer VI across the entire mediolateral extent of area 17. In normals injected with HRP on postnatal day 2 and perfused 24 h later, callosal neurons were distributed throughout the dorsal posterior neocortex, primarily in layers V and VI. Only a very few labelled cells were visible in the supragranular laminae. In adult mice blinded at birth, the zone of callosal cells and terminals extended much further into area 17 than in normals, but aside from the anterograde labelling in layer VI and lowermost lamina V, the medial one-third of the striate cortex was still for the most part devoid of callosal cells and fibers. The laminar distributions of the labelled cells and anterograde transport in the blinded animals were the same as in the normal mice. In both strains of anophthalmic mice the pattern of callosal connections was unlike that in either the normals or neonatal enucleates. In the caudal “visual” cortex, callosal cells and anterograde transport indicative of terminal labelling were visible primarily in the 17–18a border area. Rostrally, however, they were both distributed in multiple (two-three) patches within area 17. Serial reconstructions demonstrated that these patches tended to be aligned in stripes which ran parallel to the 17–18a border. One of these was always located at the 17–18a border, and here the laminar distribution of labelled cells and anterograde labelling was the same as in the normals. In the more medial patches, however, labelled cells and anterograde labelling were confined almost completely to layers II and III. The distribution of callosal cells in neonatal ZRDCT-an mice was not appreciably different from that in C57BL mice of the same age.

Notes: Summary Anterograde and retrograde labelling with the carbocyanine dye, Di-I, was used to assess the development of the visual cortical projection to the superior colliculus (SC) in pre- and postnatal hamsters. Posterior cortical axons arrive in the SC on postnatal (P-) day one (the first 24 hours after birth = P-0) and begin to arborize in the superficial laminae (the stratum griseum superficiale [SGS] and stratum opticum [SO]) within one day after they enter the tectum. Over succeeding days, the density of the projection increases and numerous labelled fibers are visible throughout the depth of the SGS and SO. Beginning on P-6, there is a decrease in the density of labelled fibers in the upper SGS and by P-10, the laminal distribution of the occipital corticotectal pathway appears adult-like. Anterograde tracing with Di-I also revealed the presence of a few corticotectal fibers that crossed the midline in both the SC and posterior commissures to terminate mainly in the superficial tectal laminae contralateral to the injection site. Crossed corticotectal fibers were visible in hamsters aged between P-3 and P-12. Retrograde tracing with Di-I in hamsters killed between P-3 and P-12 demonstrated that both the ipsilateral and crossed corticotectal projections arose exclusively from pyramidal cells in developing lamina V.