Distribution of visual callosal neurons in normal and strabismic cats

Abstract

It has been suggested that synchronous activation of cortical loci in the two cerebral hemispheres during development leads to the stabilization of juvenile callosal connections in some areas of the visual cortex. One way in which loci in opposite hemispheres can be synchronously activated is if they receive signals generated by the same stimulus viewed through different eyes. These ideas lead to the prediction that shifts in the cortical representation of the visual field caused by misalignment of the visual axes (strabismus) should change the width of the callosal zone in the striate cortex. We tested this prediction by using quantitative techniques to compare the tangential distribution of callosal neurons in the striate cortex of strabismic cats to that in normally reared cats. Animals were rendered strabismic surgically at 8-10 days of age and were allowed to survive a minimum of 18 weeks, at which time multiple intracortical injections of the tracer horseradish peroxidase (HRP) were used to reveal the distribution of callosally projecting cells in the contralateral striate cortex. HRP-labeled cells were counted in coronal sections, and data from four animals with divergent strabismus (exotropia) and four with convergent strabismus (esotropia) were compared to those from four normally reared animals. Although our data from strabismic cats do not differ markedly from those reported previously, we find that the distribution of callosal cells in the striate cortex of these cats does not differ significantly from that in our normally reared control cats. These results do not bear out the prediction that surgically shifting the visual axes leads to stabilization of juvenile callosal axons in anomalous places within the striate cortex.

Reorganization of Visual Callosal Connections Following Alterations of Retinal Input and Brain Damage

“…It is noteworthy that strabismus is effective in enlarging callosal zone even when induced as late as postnatal day 36 (Berman and Payne, 1983). However, contradictory results were also reported by other groups, that found no changes in size of callosal zone (Bourdet et al, 1996). These discrepancies could be due to different methodological experimental procedures and different onset of pathology.…”

Cross-modal reorganization of callosal connectivity without altering thalamocortical projections

“…In cat visual cortex, bilateral deprivation or enucleation result in a reduced callosal projection (44)(45)(46), whereas monocular manipulations result in expanded callosal projections (16,47,48). However, binocularity seems not to play an important organizing role in this pathway, since strabismus does not affect the pattern or number of callosal cells (49,50). Rather, the outcome of deafferentation is predicted by the effect of the manipulation on retinotopic correspondence between the two hemispheres (18,19,44,49,50).…”

“…However, binocularity seems not to play an important organizing role in this pathway, since strabismus does not affect the pattern or number of callosal cells (49,50). Rather, the outcome of deafferentation is predicted by the effect of the manipulation on retinotopic correspondence between the two hemispheres (18,19,44,49,50). In deaf animals, there may be no information available on which to base elimination of connections, as in the retention of overlapped corticocortical (51) or thalamocortical (52) arbors after visual deprivation.…”

Asymmetrical Interhemispheric Connections Develop in Cat Visual Cortex after Early Unilateral Convergent Strabismus: Anatomy, Physiology, and Mechanisms

“…At the present time, some authors claim that strabismus leads to extended distribution of cell bodies of callosal neurons in one or both hemispheres through the stabilization of juvenile exuberant ones (Innocenti and Frost, 1979; Berman and Payne, 1983; Elberger et al, 1983). But other authors do not agree with this view (Lund et al, 1978; Bourdet et al, 1996). The same conclusion has also been proposed for callosal terminals (Lund et al, 1978; Lund and Mitchell, 1979; Berman and Payne, 1983).…”

“…Subsequent development of CC in cat visual cortex was investigated at the level of callosal terminals by combining electrophysiology and tracer injection techniques. Although controversial, some anatomical data in the literature have already suggested that procedure this may lead to asymmetric callosal connections in one hemisphere and the other in adulthood (Lund and Mitchell, 1979; Berman and Payne, 1983; but see Elberger et al, 1983; Bourdet et al, 1996). …”