Projection In Hamsters Research Articles

Organization of the corticotectal projection in hamsters with neonatally elevated levels of serotonin in the superior colliculus

A previous study from this laboratory showed that elevated serotonin (5-HT) levels in the hamsters superior colliculus (SC), induced by a single subcutaneous injection of 5,7-dihydroxytryptamine (5,7-DHT) at birth, resulted in an abnormally widespread distribution of the uncrossed retinotectal projection. The present study investigated whether the corticotectal projection in such animals was altered. Adult normal and 5,7-DHT-treated hamsters were injected with horseradish peroxidase (HRP) into occipital cortex and processed for anterograde tracing of corticotectal terminals in the SC. Quantitative analysis showed that normal and 5,7-DHT-treated hamsters were not significantly different in total labeling or in the gradient of labeling density within the SC. These data indicate that corticotectal axons achieve normal terminal fields after neonatal elevation of 5-HT in the SC.

The early development of thalamocortical and corticothalarnic projections

The early development of thalamocortical and corticothalamic projections in hamsters was studied to compare the specificity and maturation of these pathways, and to identify potential sources of information for specification of cortical areas. The cells that constitute these projections are both generated prenatally in hamsters and they make reciprocal connections. Fluorescent dyes (DiI and DiA) were injected into the visual cortex or lateral geniculate nucleus in fixed brains of fetal and postnatal pups. Several issues in axonal development were examined, including timing of axon outgrowth and target invasion, projection specificity, the spatial relationship between the two pathways, and the connections of subplate cells. Thalamic projections arrive in the visual cortex 2 days before birth and begin to invade the developing cortical plate by the next day. Few processes invade inappropriate cortical regions. By postnatal day 7 their laminar position is similar to mature animals. By contrast, visual cortical axons from subplate and layer 6 cells reach posterior thalamus at 1 day after birth in small numbers. By 3 days after birth many layer 5 cell projections reach the posterior thalamus. On postnatal day 7, there is a sudden increase in the number of layer 6 projections to the thalamus. Surprisingly, these layer 6 cells are precisely topographically mapped with colabeled thalamic afferents on their first appearance. Subplate cells constitute a very small component of the corticothalamic projection at all ages. Double injections of DiI and DiA show that the corticofugal and thalamocortical pathways are physically separate during development. Corticofugal axons travel deep in the intermediate zone to the thalamic axons and are separate through much of the internal capsule. Their tangential distribution is also distinct. The early appearance of the thalamocortical pathway is consistent with an organizational role in the specification of some features of cortical cytoarchitecture. The specific initial projection of thalamocortical axons strongly suggests the recognition of particular cortical regions. The physical separation of these two pathways limits the possibility for exchange of information between these systems except at their respective targets.

Identification of synapses formed by the aberrant, uncrossed retinogeniculate projection in the hamster after neonatal monocular enucleation.

The terminals of the abnormally enhanced, stabilized uncrossed retinogeniculate projection in adult hamsters produced by removal of one eye at birth, were labelled by injection of HRP into the remaining eye and examined by electron microscopy. Labelled terminals closely resembling normally positioned retinal terminals were found to make well-differentiated synaptic contacts with geniculate projection and interneuron-like cells in regions of the dorsal lateral geniculate nucleus that do not receive uncrossed retinal input in normal adult animals.

Effects of neonatal cortical lesions upon retinocollicular projections in the hamster

Autoradiography and anterograde horseradish peroxidase transport were used to examine retinocollicular projections in normal hamsters and in animals subjected to ablation of the ipsilateral, posterior neocortex at 1, 3, 6, 10 or 120 days of age. The crossed retinotectal projections of all groups were quite similar. There did, however, appear to be a slight increase in the density of the projection to the lower portion of the stratum griseum superficiale in the neonatally brain-damaged hamsters. The uncrossed pathway, on the other hand, was quite abnormal in the neonatally lesioned animals. In normals, the ipsilateral retinocollicular projection consisted almost entirely of a series of patches along the stratum yriseum superficiale-stratum opticum border in the rostral one-third of the colliculus. Only a few axons from the ipsilateral eye were observed in the caudal two-thirds of the tectum and these could only be visualized when horseradish peroxidase was used as the tracer. In all of the neonatally brain-damaged hamsters both autoradiography and horseradish peroxidase tracing demonstrated that the ipsilateral retina densely innervated the entire rostrocaudal extent of the colliculus. Retrograde tracing experiments demonstrated that the portion of the temporal retina which gave rise to the uncrossed retinocollicular projection in the normal hamsters was also the source of the expanded projection in the neonatally brain-damaged animals; and, further, that the numbers and areal distributions of ipsilaterally projecting retinal and retinocollicular ganglion cells were similar in the two groups. These findings suggest that, at least in the hamster, normal inputs from the two eyes may not be a sufficient condition for the development of the largely complementary pattern of collicular innervation by the two retinae.

Compressed retinotectal projection in hamsters: fewer ganglion cells project to tectum after neonatal tectal lesions.

After partial ablation of the superior colliculus (tectum) in neonatal hamsters, the whole extent of the visual field comes to be represented in a compressed map on the remaining tectal fragment. However, the total volume of tectal tissue in which retinotectal fibers arborize is less than normal. These observations suggests that the retinal ganglion cells which arborize in this reduced volume might arise throughout the whole extent of the retina but be fewer in number than normal. Alternatively, the ganglion cells which project to the tectum might be normal in number but reduced in terminal arbor size. To distinguish between these possibilities, we have used tectal injections of horseradish peroxidase to label retinal ganglion cells which project to the tectum. The numbers of labelled cells per mm2 of retina were counted in selected regions. In hamsters with small lesions, which left 80--85% of the tectum intact, the density of labelled retinal ganglion cells was normal. However, in hamsters with larger lesions, the density of labelled cells was significantly lower than normal.

Expansion of the ipsilateral visual corticotectal projection in hamsters subjected to partial lesions of the visual cortex during infancy: anatomical experiments.

Electrophysiological methods were employed to determine whether or not partial visual cortical lesions in neonatal (7--11-day) hamster produced large scotomas in the cortical visual representation. In cases where such scotomas were present electrophoretic deposits of radioactive amino acids in the visually responsive "cortical remnant" of the damaged hemisphere resulted in labelling throughout the lower portion of the stratum griseum superficiale and the stratum opticum of the ipsilateral superior colliculus. No differential labeling of the part of the colliculus which was topographically matched with the remaining visual representation in the cortical remnant was observed. In normal hamsters relatively localized, visual cortical deposits of radioactive amino acids resulted in superficial layer labeling only in portions of the colliculus which corresponded to the locus of the cortical deposit. In a similar fashion, small lesions at physiologically defined loci in the cortical remnant produced degeneration throughout most of the superficial tectal laminae, but a more restricted "focus" of denser degeneration was also visible in these cases. The position of this focus in the colliculus for a given cortical lesion varied with the nature of the visual map in the cortical remnant. In several additional neonatally brain-damaged hamsters large lesions of the visual cortex in the intact hemisphere were combined with radioactive amino acid deposits in the cortical remnant to determine whether or not axons from the crossed corticocollicular pathway previously demonstrated in such hamsters were intermingled with fibers from the ipsilateral corticotectal projection. In alternate sections processed for autoradiography or by the Fink-Heimer ('67) method autoradiographic label and degeneration argyrophilia were both observed in the medical part of the colliculus ipsilateral to the neonatal cortical lesion.

Expansion of the ipsilateral visual corticotectal projection in hamsters subjected to partial lesions of the visual cortex during infancy: Electrophysiological experiments

Single unit recording from cells in the superior colliculus ipsilateral to the damaged hemisphere in hamsters subjected to unilateral removal of a part of the posterior neocortex during infancy was combined with electrical stimulation of the cortical remnant and the visual cortex in the undamaged hemisphere. Cells activated by stimulation of the cortical remnant were recorded in all portions of the colliculus. No differences in percentages of driven cells or threshold current intensities were noted between electrode penetrations in which collicular neurons having receptive fields within the remaining visual cortical representation were recorded and tracks where units with receptive fields outside this region were isolated. In the medical part of the tectum ipsilateral to the damaged hemisphere cells driven by stimulation of either cortex were encountered. It was also demonstrated that stimulation of the ipsilateral cortical remnant and/or the contralateral cortex was capable of suppressing discharges normally elicited by optic chiasm or visual stimulation in a manner qualitatively similar to that observed for collicular cells in normal hamsters. The response properties of cells functionally influenced by the ipsilateral and/or contralateral corticles were not different from those of neurons which received no demonstrable cortical input. The receptive field characteristics of the sample of neurons recorded were, on the whole, quite similar to those of collicular neurons in hamsters subjected to lesions of the visual cortex as adults.