scholarly journals Postnatal development and plasticity of corticocortical projections from area 17 to area 18 in the cat's visual cortex

1994 ◽  
Vol 14 (5) ◽  
pp. 2747-2762 ◽  
Author(s):  
DJ Price ◽  
JM Ferrer ◽  
C Blakemore ◽  
N Kato
1999 ◽  
Vol 16 (1) ◽  
pp. 35-44 ◽  
Author(s):  
FERNANDO PÉREZ-CERDÁ ◽  
LUIS MARTÍNEZ-MILLÁN ◽  
CARLOS MATUTE

We have studied the postnatal development of presumptive axon terminals (puncta) which were recognized by antibodies to the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) and were located on the somata of area 17 neurons projecting to the ipsilateral area 18 of the visual cortex in cats ranging from 7 days of age to adulthood. Projection neurons were retrogradely labeled by injection of horseradish peroxidase conjugated to wheat germ agglutinin into the ipsilateral area 18. These neurons were mainly pyramidal in shape at all the developmental stages examined and the adult distribution of labeled cells was reached by 21 days. Subsequent GABA postembedding immunohistochemistry using high-resolution light microscopy was carried out to study the development of GABAergic terminals on cell bodies of identified projecting neurons in layers II–III. At all ages examined, we found perisomatic GABAergic puncta on these cells. Their density showed a significant increase from postnatal days 7 to 45, and then remained largely constant through adulthood. Since GABAergic puncta are considered the light-microscopic correlate of GABAergic synaptic terminals, our results support the idea of a developmentally regulated increase in the inhibitory activity of local interneurons on area 17 pyramidal neurons projecting to area 18 in the cat visual cortex which occurs within the same time frame as that of the acquisition of the mature operation of these cells.


Retrogradely transported tracers were injected into area 18 of the visual cortex of the adult cat to study the organization of corticocortical projections from area 17 to area 18. All injections, whether very small or relatively large, and irrespective of their exact location in area 18, produced a discontinuous, clustered distribution of labelled cells, mainly in layers II, III and upper IV, in a topographically related region of area 17. The mean centre–centre distance between neighbouring patches was about 750 μm. We conclude that the overall population of cells projecting to area 18 is genuinely distributed in a patchy fashion and that they provide an efficient spatial sample of information from area 17. Comparison of the dimensions of each injection site and of the retrogradely labelled territory suggested that each region in area 18 receives a convergent input from a zone in area 17 whose visual field representation is about 0.8 M –1 deg larger in all directions (where M is the magnification factor in millimetres per degree at the termination site in area 18). Pairs of injections were made in area 18 by placing small volumes of two fluorescent tracers, fast blue and diamidino yellow, side-by-side in either a rostrocaudal or a mediolateral plane, with different distances between them. When the boundaries of the dense central cores of two injection sites were separated, at their closest points, by about 1.6 mm, the two corresponding distributions of labelled cells in area 17 were just non-overlapping, suggesting that each group of cells in area 17 sends a divergent projection to innervate a zone about 0.8 mm larger in all directions in area 18. More closely spaced injections led to overlap of the distributions of labelling by the two dyes, with shared clusters containing a mixture of labelled cells. The proportion of double-labelled cells in these shared clusters never exceeded 4.4% (but was 70% after sequential injection of the two dyes at a single point). We conclude that, although each cluster of cells sends a divergent projection to area 18, the majority of individual axons terminate more discretely, perhaps providing specific inter-connections between functionally corresponding ‘columns’ in the two areas.


1993 ◽  
Vol 54 (2) ◽  
pp. 205-210 ◽  
Author(s):  
N. Kato ◽  
J.M.R. Ferrer ◽  
D.J. Price ◽  
C. Blakemore

1999 ◽  
Vol 82 (5) ◽  
pp. 2667-2675 ◽  
Author(s):  
Susana Martinez-Conde ◽  
Javier Cudeiro ◽  
Kenneth L. Grieve ◽  
Rosa Rodriguez ◽  
Casto Rivadulla ◽  
...  

In the absence of a direct geniculate input, area 17 cells in the cat are nevertheless able to respond to visual stimuli because of feedback connections from area 18. Anatomic studies have shown that, in the cat visual cortex, layer 5 of area 18 projects to layer 5 of area 17, and layers 2/3 of area 18 project to layers 2/3 of area 17. What is the specific role of these connections? Previous studies have examined the effect of area 18 layer 5 blockade on cells in area 17 layer 5. Here we examine whether the feedback connections from layers 2/3 of area 18 influence the orientation tuning and velocity tuning of cells in layers 2/3 of area 17. Experiments were carried out in anesthetized and paralyzed cats. We blocked reversibly a small region (300 μm radius) in layers 2/3 of area 18 by iontophoretic application of GABA and recorded simultaneously from cells in layers 2/3 of area 17 while stimulating with oriented sweeping bars. Area 17 cells showed either enhanced or suppressed visual responses to sweeping bars of various orientations and velocities during area 18 blockade. For most area 17 cells, orientation bandwidths remained unaltered, and we never observed visual responses during blockade that were absent completely in the preblockade condition. This suggests that area 18 layers 2/3 modulate visual responses in area 17 layers 2/3 without fundamentally altering their specificity.


1993 ◽  
Vol 93 (2) ◽  
Author(s):  
J.M. Alonso ◽  
J. Cudeiro ◽  
R. P�rez ◽  
F. Gonzalez ◽  
C. Acu�a

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.


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