The intrinsic, association and commissural connections of area 17 of the visual cortex

Abstract

An experimental neurohistological study has been made of the intrinsic connections of the cortex of area 17 of the monkey, of the commissural connections of the visual cortex of the cat and monkey and of the association fibres passing into area 17 of the cat. In light microscopic studies the axonal degeneration method of Nauta has been used, and the site and mode of termination of the degenerating fibres has also been determined with the electron microscope. After narrow slit lesions through the depth of the cortex of area 17 degeneration of the intrinsic fibre connections does not extend beyond 5-6 m m : this extent is asymmetrical, being 1-2 mm further on one side of the lesion than on the other. In all layers there is intense fine degeneration in a width of 200 jxm on each side of the lesion and in layer IV no degeneration extends beyond this distance. In all the other layers there is moderate fibre and terminal degeneration for up to 2 mm on one side and 1 mm on the other; in the stria of Gennari fibre degeneration continues for a further 1-2 mm from the lesion, and these fibres probably terminate within the stria and in the immediately adjoining parts of layer I llb superficially and in layer IV deeply. After a small focal lesion in layers I and II fine degeneration is found in these layers over a total extent of 2-3 mm, and a few fibres pass down into layer III. When the damage extends into layer III, in addition to the horizontal degeneration in this layer there is a moderate degree of fibre degeneration in the stria, in layers V and VI and a few fibres pass into the underlying white matter. If the lesion extends deep enough to involve the stria dense horizontal fibre degeneration appears in it and this extends to a maximum width of 5-6 mm. Similar degeneration in the stria has been found after small lesions restricted to it or within layer IV, indicating that most of the horizontal fibres in the stria arise within the cortex and probably in layer IV (or V and VI). When the lesion reached down to layer V there was an increase in the density of degeneration in layer V itself, in layers II and III, and more degenerating fibres entered the white matter; these observations suggest that many of the fibres in layer V arise in that layer, that there is a recurrent projection from layer V to layers II and III and that most of the efferent fibres from area 17 arise in the deep layers of the cortex. Degenerating fibres which pass vertically up or down from a small lesion in the cortex were confined to a narrow band lying above or below the lesion. Electron microscopic observations are in good agreement with the light microscopy both with respect to the extent of the degeneration and with the variation in the different laminae. The degenerating axon terminals formed only a small proportion of the total number of terminals present, and there was a marked decrease in their number beyond 1 mm from the lesion. The majority (90 %) of the terminals had asymmetrical membrane thickenings and most made contact with dendritic spines; others formed synapses upon dendrites and cell somata of stellate cells. Degenerating terminals with symmetrical membrane thickenings formed 10 % of the total and the post-synaptic profiles related to these were complementary to those of the asymmetrical terminals, 78 % ending on dendrites of both pyramidal and non-pyramidal cells. A small number ended on cell bodies and on initial segments. The degeneration of commissural fibres was studied only at the boundary of areas 17 and 18. With the light microscope it was found that all layers were affected by degeneration in area 18 but that layer IV was clear in area 17. This was confirmed with the electron microscope and it was found that all of the terminals had asymmetrical membrane thickenings and the majority made synaptic contact with dendritic spines. The association fibre connections passing from area 18 into area 17 of the cat were found to terminate only in the lateral part of area 17 and that layer IV was left clear of fragmentation. These fibres have asymmetrical terminals and the majority end on dendritic spines.