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Title: An investigation of certain connections of the visual cortex
Author: Fisken, R. A.
ISNI:       0000 0001 3467 727X
Awarding Body: University of Oxford
Current Institution: University of Oxford
Date of Award: 1975
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In recent years our understanding of the functional properties of mammalian sensory cortex has advanced considerably, and it has been possible to correlate some of the physiological findings with certain anatomical features. At present, however, there is little anatomical evidence available concerning the columnar arrangement of cortical cells and the apparently high degree of specificity of connections between them. In an attempt to elucidate certain of these problems, material has been studied from the visual cortex (area 17) of rhesus monkeys. In addition, observations have been made on the commissural connections to the cortex at the boundary of areas 17 and 18 in the cat and monkey and on the association fibre projection from area 18 to area 17 in the cat. Intrinsic connections within area 17 of the monkey Small lesions were placed in the cortex of area 17, either with a needle or fine scalpel (slit lesions) or with a tungsten microelectrode, and the animals were allowed to survive for periods of 1-6 days. For light microscopy the occipital lobes were sectioned, in either the coronal or sagittal plane, at 25 μm. Sections were stained by the Nauta-Gygax, Fink-Heimer or Wiitanen method. For electron microscopy, small blocks of tissue of 1-2 cu. mm volume were taken and embedded in Epon- Araldite. One μm 'thick' sections, perpendicular to the pial surface, wore cut from the whole blocf face. Areas for thin sections were chosen so that, when maps of several areas were fitted together, they would form an almost complete representation of the whole depth of the cortex extending out from the lesion for 3 mm. With the light microscope, axonal degeneration after lesions through the depth of the cortex is seen to extend for only a few millimetres from the site of the lesion, and in almost all cases this extent is asymmetrical, being 1.0-1.5 mm further on one side of the lesion than the other. Except for approximately 200 μm on each side, where there is dense, fine terminal degeneration throughout ail layers, there are distinct differences both in the appearance and the extent of the degeneration in different laminae. In layer I there is a little fine granularity and a few degenerating fibres distributed over a few millimetres from the lesion. Layers II and III resemble each other in showing an even distribution of fine, granular degeneration which is dense for only up to 200 μm on either side, after which it remains more or less uniform for a distance of about 1.5 mm, when it stops rather suddenly. On its deep aspect this degeneration is continuous with marked horizontal fibre and terminal degeneration in the stria of Gennari in layer IIIc, and the extent of this axonal degeneration is the greatest of all, reaching up to 4 mm away and apparently terminating in layer IIIc and the adjacent parts of layers IIIb and IV. Layer IV shows no degeneration except for a zone of some 200 μm immediately adjacent to the lesion, where there is dense granularity. Layer V shows an appearance similar to that of the stria, except that the fibre and terminal degeneration is coarser in V and extends in any quantity for only 1 mm or so from the lesion, being very sparse thereafter. Layer VI is again similar but shows many more obliquely arranged fibres so that there is no appearance of a horizontal fibre band comparable to those in IIIc and V (bands of Baillarger). The pattern of degeneration after lesions which extend into the underlying white matter differs from the above description only in that there is more fibre degeneration in the deep layers and the terminal degeneration in layer IV is more widespread on the side of the lesion away from the direction from which the thalamocortical fibres approach. The laminar origin of intrinsic axons was determined by lesions which involved only some of the layers of the cortex or which were in the form of discrete microelectrode lesions in individual laminae. Lesions restricted to layers I and II produced only local degeneration which was mainly granular and reached no deeper than the bottom of layer IIIa. Extension of the lesion down to the bottom of layer IIIb produced only a modest increase in the horizontal extent of the degeneration, which now reached to about 1.5 mm from the lesion. Deep to the lesion, degeneration was seen in layers IIIc, IV and V; however, that in IIIc, in the stria, was only of the same extent and density as in the rest of layer III, while that in layer IV took the form of vertically oriented fibres going down to a patch of granularity in layer V. A few degenerating fibres were seen to leave the cortex. Thus it seems that cells in the supragranular layers give off intrinsic projections only to the immediately adjoining region for a distance of about 1.5 mm, and there is no evidence that the projection of supragranular cells into the stria of Gennari is anything more than small in amount and rather restricted in extent. Some cells in layer III project to layer V, though this projection does not appear to be particularly dense. Only a few degenerating axons descend into the white matter. When the lesion reached the stria of Gennari there was a sudden increase in both the density and extent of degeneration in that layer, and this degeneration was very similar to that seen after a lesion through the whole depth of the cortex. Involvement of layer IV gave rise to a pattern which was essentially the same as that resulting from lesions of the stria, and even a small focal lesion of layer IV produced fairly dense, extensive degeneration in layer IIIc. These results suggest that much of the stria is made up of the horizontal ramifications of ascending axons, and that many of these fibres arise from granule cells in layer IV; some may arise from cells of layer IIIc itself or may be axon collaterals of cells in layers V and VI. When the lesion reached down to layer V there was an increase in the amount of terminal degeneration in layer IV and in the density and extent oi degeneration in the inner band of Baillarger in layer V. In addition, more degenerating fibres could be seen entering the white matter. Thus the cells of layer V appear to send axonal branches into the inner bane: of Baillarger for about 1 mm; since the apical dendrites of these cells may receive a thalamic input, this projection may be related to the further processing of information by infragranular complex and hypercomplex cells. The cells of layers V and VI also project to the white matter and give rise to ascending collaterals to more superficial layers. The observations with the electron microscope were in good agreement with the light microscope findings; in particular, the rather restricted extent of the degeneration and the variations in density and extent of degeneration between the different laminae were shown. Some clustering of degenerating terminals was apparent, though it was not very marked. It is worthy of note that the terminals which degenerate after an intrinsic lesion of the cortex form only a small proportion of the total number of terminals present. This may seem surprising, but several important considerations apply: the cells projecting horizontally to a given point will be distributed throughout a very restricted region around it, so that a lesion would have to be very close to that point in order to destroy more than a small fraction of all of its horizontal connections. When it is also considered that many connections to a point may travel vertically and that degenerating terminals could be identified with the electron microscope only ii certain criteria were satisfied, the apparently low yield of terminals in our material becomes readily understandable.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available