Journal of Neuroscience, Vol 14, 2747-2762, Copyright © 1994 by Society for Neuroscience
Postnatal development and plasticity of corticocortical projections from area 17 to area 18 in the cat's visual cortex
DJ Price, JM Ferrer, C Blakemore and N Kato
Department of Physiology, University Medical School, Edinburgh, United Kingdom.
We used retrogradely transported fluorescent tracers to study the
development of projections from area 17 to area 18 in normal and
monocularly deprived kittens. In newborn animals, cells in area 17 that
were labeled from small, discrete injections in area 18 were concentrated
around the retinotopically corresponding zone, but distributed with lower
density over a very wide surrounding area. Hence, the total convergence and
divergence of the projection were initially enormous, but they decreased
dramatically, mainly during the first postnatal month, through elimination
of the sparse, widespread distribution of projections. Injections of two
different tracers close together in area 18 produced very few
double-labeled cells in area 17 at any age, implying that most individual
axons arborize over very small territories even at birth. In normal kittens
the peak density of association cells in the upper layers, corrected for
the overall expansion of the cortex, doubled over the first postnatal month
and then declined gradually over the following several months, presumably
because of continuing selection and elimination. As shown in previous work
(Price and Blakemore, 1985a), area 17 to 18 cells in newborn kittens were
distributed in two continuous bands in supragranular and infragranular
layers. During normal maturation, elimination of projections results in the
formation of distinct clusters; these lie preferentially in the upper
layers above patches of ipsilateral eye input to layer 4 (Price et al.,
1994). Monocular deprivation, which causes the terminal patches
representing the deprived eye to become much smaller than normal, did not
stop the normal decrease in overall convergence/divergence or the
appearance of clusters of association cells, but the clusters were
distinctly larger than normal in both hemispheres. Monocular deprivation
also prevented the normal reduction in density of association cells within
clusters after 1 month of age. Comparison with results from binocularly
deprived animals, where clusters also form but association cell density is
low, suggests that the size of clusters and the density of association
cells retained depend on the overall level of cortical activity.