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Normal and abnormal uncrossed retinotectal pathways in rats: An HRP study in adults
Author(s) -
Lund R. D.,
Land P. W.,
Boles J.
Publication year - 1980
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/cne.901890407
Subject(s) - superior colliculus , retina , biology , tectum , anatomy , superior colliculi , enucleation , neuroscience , midbrain , retrograde tracing , ganglion , giant retinal ganglion cells , retinal , visual system , retinal ganglion cell , soma , central nervous system , biochemistry , genetics
Horseradish peroxidase was injected into the superior colliculus of normal pigmented and albino rats and rats which had been unilaterally enuleated at birth, in order to identify the retinal ganglion cells which contribute normal and abnormal uncrossed retinotectal axons. The results show that while in pigmented rats, the normal uncrossed pathway derives solely from the lower temporal retina and distributes to the anterior and medial parts of the colliculus, occasional cells throughout the retina of albino rats contribute to the uncrossed pathway and the terminal distribution is broader in the tectum. These findings are confirmed with orthograde pathway tracing methods. After neonatal unilateral eye enucleation, many more ganglion cells in the remaining eye of both pigmented and albino rats project ipsilaterally. It is notable from both HRP studies and from further degenration experiments that cells in part of the lower temporal retina do not restrict their distribution to a mirror togographic position in the ipsilateral tectum but send axons across all but the posterolateral part of the colliculus. No single class of ganglion cell (defined by soma diameter) appears responsible for the expanded ipsilateral projection, although more large cells from the lower temporal retina are involved. These may be the result of enlargement of cells with expanded terminal fields rather than necessarily indicating a preferential contribution from one retinal ganglion cell class.