Influence of layer V of area 18 of the cat visual cortex on responses of cells in layer V of area 17 to stimuli of high velocity

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


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.


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.


1991 ◽  
Vol 66 (5) ◽  
pp. 1667-1679 ◽  
Author(s):  
D. Ferster ◽  
B. Jagadeesh

1. Nonlinearity of spatial summation in areas 17 and 18 of cat visual cortex was compared with the type of spatial nonlinearity that differentiates X and Y cells in the lateral geniculate nucleus (LGN) and retina. The comparisons were made to examine to what extent the information from X and Y cells may remain separated in higher visual centers. 2. Responses of simple cells in areas 17 and 18 were recorded while stationary, optimally oriented sinewave gratings were sinusoidally modulated within the receptive field of the cell. Both the spatial frequency and spatial phase of the stimulus were varied. 3. Y cells in the retina and LGN are defined by the presence of a specific form of spatial nonlinearity. When tested with contrast-modulated sinewave gratings of spatial frequencies about three-fold greater than the optimal, their responses are dominated by a frequency-doubled component. The amplitude of the frequency-doubled component is not dependent on the spatial phase of the stimulus. 4. Many simple cells in the cortex showed a form of spatial nonlinearity similar to the defining nonlinearity found in retinal and geniculate Y cells. A frequency-doubled response dominated at spatial frequencies more than threefold greater than the optimal spatial frequency. When this response was present, it was phase independent. 5. More than 50% of the simple cells in area 18 showed the Y-like spatial nonlinearity. Fewer than 10% of the simple cells in area 17 showed the Y-like spatial nonlinearity. 6. The virtual absence of Y-like nonlinearity in area 17 and its relative abundance in area 18 suggest that the functional separation between the parallel X and Y pathways remains distinct within areas 17 and 18 of cat visual cortex.


The thalamic projection to the visual cortex has been studied in the cat and monkey by experimental light and electron microscopic techniques. After large lesions of the lateral geniculate nucleus degeneration is confined to the ipsilateral hemisphere. In the cat it is found in areas 17, 18 and 19 and in the lateral suprasylvian area, terminal degeneration occurring predominantly in layer IV, with less in layers I, III and V ; fibre degeneration crossing layers VI and V towards layer IV is coarser in area 18 than elsewhere. Some fine horizontal degenerating fibres are seen in layer I. In the monkey terminal degeneration is restricted to area 17; again degenerating fibres ascend to layer IV where there is dense fragmentation, but in contrast to the cat there is also a second, less dense, but distinct, band in layer Illb. A little fine, horizontal fibre degeneration is present in layer I and there is slight terminal degeneration in this site and in layer V. Electron microscopy shows that degenerating terminals are recognizable in the visual cortex at several stages according to survival period, but that most stages can exist simultaneously in any one site, and that all are associated with asymmetrical membrane thickenings. Mapping of electron microscopic sections confirms the laminar pattern seen with the light microscope. In area 17 of the cat and monkey and in area 19 of the cat over 80% of degenerating terminals end on dendritic spines, the rest making synaptic contact mainly with dendritic shafts, and very few with the soma of stellate cells, but in area 18 some 10 % are related to stellate cell bodies. In layer IV of all areas degenerating terminals tend to occur in clusters which are separated by approximately 100 μ m. Where degenerating thalamic afferents end on cell somata or varicose dendrites almost all are identifiable as derived from stellate cells. Although it is difficult to identify positively the parent dendrites bearing the spines which receive the majority of the thalamo-cortical afferents, it is suggested that some, at least, of them may also originate from stellate cells.


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