PubMed Health⌕ Search

Biomedical subjects

R E Kalil

Publications and source records attributed to R E Kalil.

At least 19 recordsLinked to original sources
PubMed1991

Thalamic projections to the lateral suprasylvian visual area in cats with neonatal or adult visual cortex damage.

Previous transneuronal anterograde tracing studies have shown that the retino-thalamic pathway to the posteromedial lateral suprasylvian (PMLS) visual area of cortex is heavier than normal in adult cats that received neonatal damage to visual cortical areas 17, 18, and 19. In contrast, the strength of this projection does not appear to differ from that in normal animals in cats that experienced visual cortex damage as adults. In the present study, we used retrograde tracing methods to identify the thalamic cells that project to the PMLS cortex in adult cats that had received a lesion of visual cortex during infancy or adulthood. In five kittens, a unilateral visual cortex lesion was made on the day of birth, and horseradish peroxidase (HRP) was injected into the PMLS cortex of both hemispheres when the animals were 10.5 to 13 months old. For comparison, HRP was injected bilaterally into the PMLS cortex of three cats 6.5 to 13.5 months after they received a similar unilateral visual cortex lesion as adults. In cats with a neonatal lesion, retrograde labeling was found in the large neurons that survive in the otherwise degenerated layers A and A1 of the lateral geniculate nucleus (LGN) ipsilateral to the lesion. Retrograde labeling of A-layer neurons was not seen in the undamaged hemisphere of these animals or in either hemisphere of animals that had received a lesion as adults. As in normal adult cats, retrograde labeling also was present in the C layers of the LGN, the medial interlaminar nucleus, the posterior nucleus of Rioch, the lateral posterior nucleus, and the pulvinar nucleus ipsilateral to a neonatal or adult lesion. Quantitative estimates indicate that the number of labeled cells is much larger than normal in the C layers of the LGN ipsilateral to a neonatal visual cortex lesion. Thus the results indicate that the heavier than normal projection from the thalamus to PMLS cortex that exists in adult cats after neonatal visual cortex damage arises, at least in part, from surviving LGN neurons in the A and C layers of the LGN. Although several thalamic nuclei, as well as the C layers of the LGN, continue to project to PMLS cortex after an adult visual cortex lesion, these projections appear not to be affected significantly by the lesion.

Aging↗
PubMed1991

Development of the projections from the dorsal lateral geniculate nucleus to the lateral suprasylvian visual area of cortex in the cat.

In the study reported in the preceding paper, we used retrograde labeling methods to show that the enhanced projection from the thalamus to the posteromedial lateral suprasylvian (PMLS) visual area of cortex that is present in adult cats following neonatal visual cortex damage arises at least partly from surviving neurons in the dorsal lateral geniculate nucleus (LGN). In the C layers of the LGN, many more cells than normal are retrogradely labeled by horseradish peroxidase (HRP) injected into PMLS cortex ipsilateral to a visual cortex lesion. In addition, retrogradely labeled cells are found in the A layers, which normally have no projection to PMLS cortex in adult cats. The purpose of the present study was to investigate the mechanisms of this enhanced projection by examining the normal development of projections from the thalamus, especially the LGN, to PMLS cortex. Injections of HRP were made into PMLS cortex on the day of birth or at 1, 2, 4, or 8 weeks of age. Retrogradely labeled neurons were present in the lateral posterior nucleus, posterior nucleus of Rioch, pulvinar, and medial interlaminar nucleus, as well as in the LGN, at all ages studied. Within the LGN of the youngest kittens, a small number of retrogradely labeled cells was present in the interlaminar zones and among the cells in the A layers that border these zones. Such labeled cells were virtually absent by 8 weeks of age, and they are not found in normal adult cats. Sparse retrograde labeling of C-layer neurons also was present in newborn kittens.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1990

The influence of action potentials on the development of the central visual pathway in mammals.

The development of the mammalian visual system begins prenatally at distributed sites, where cells generated at different embryonic ages are destined to interconnect and form the visual pathways, and ends postnatally with the functional tuning of neuronal receptive-field properties. It is reasonable to assume that the earliest stages in this developmental sequence are completed prior to the onset of neural activity, and also that activity may play only a minor role or even none at all in primary axon outgrowth and pathway finding (Harris, 1981; Harris and Holt, 1990). However, recent evidence indicates that subsequent events in development, such as the sorting of axons at their targets, the cellular differentiation of target cells and the formation of synaptic contacts by developing axons, are all influenced by action potentials. Action potentials in the developing retino-geniculo-cortical pathway can be eliminated by blocking the voltage-gated sodium channel with tetrodotoxin. Prenatal blockade prevents the laminar segregation of retinogeniculate axons. Postnatal blockade interrupts the formation of retinogeniculate synaptogenesis, slows the cytoarchitectonic differentiation of the lateral geniculate nucleus and produces abnormalities in the responses of lateral geniculate neurons. In the visual cortex, the development of cells and synapses is retarded and the eye-specific separation of geniculocortical axons is halted, thereby blocking the formation of ocular dominance columns. While the cellular mechanisms underlying these effects are not understood, a partial restoration of normal development can be produced by stimulating blocked axonal pathways electrically.

Action Potentials↗
PubMed1989

Synaptic connections between corticogeniculate axons and interneurons in the dorsal lateral geniculate nucleus of the cat.

Anatomical evidence is provided for direct synaptic connections by axons from visual cortex with interneurons in lamina A of the cat's dorsal lateral geniculate nucleus. Corticogeniculate axon terminals were labeled selectively with 3H-proline and identified by means of electron microscopic autoradiography. Interneurons in the lateral geniculate nucleus were stained with antibodies that had been raised against gamma aminobutyric acid (GABA). We found that corticogeniculate terminals synapsed with dendrites stained positively for GABA about three times as often as with unstained dendrites. Of the corticogeniculate terminals that contacted GABA-positive dendrites, 97% made synaptic connections with dendritic shafts. Only 3% synapsed with F profiles, the vesicle-filled dendritic appendages characteristic of lateral geniculate interneurons. These results suggest that the corticogeniculate pathway in the cat is directed primarily at interneurons and is organized synaptically to influence the integrated output of these cells, rather than the local interactions in which their dendritic specializations participate.

Animals↗
PubMed1987

Development of corticogeniculate synapses in the cat.

The development of corticogeniculate synapses was studied in 16 cats ranging in age from newborn to adult. Tritiated proline was injected into areas 17 and 18 of the visual cortex in order to label corticogeniculate terminals in lamina A of the dorsal lateral geniculate nucleus. The labeled terminals were then characterized ultrastructurally using electron microscopic autoradiography. Labeled synaptic profiles were found in newborn kittens, indicating that corticogeniculate connections are present in the cat at birth. Morphologically, however, many corticogeniculate endings in newborn and 1-week-old kittens are different from those in older animals in that they do not form well-defined terminal boutons, and their synaptic vesicles are often loosely packed. In kittens 2 weeks of age and older, corticogeniculate axons end as RSD terminals exclusively; i.e., they are relatively small in size and contain round, densely packed synaptic vesicles, and occasionally an electron-dense mitochondrion (Guillery: Z. Zellforsch. 99: 1-38, '69). However, not all RSD terminals in the LGN represent input from visual cortex. Injections of 3H-proline into the mesencephalic reticular formation also label RSD terminals selectively in the lateral geniculate nucleus. At all ages corticogeniculate axons make synaptic contacts with dendrites exclusively, and they are always presynaptic. This suggests that the essential pattern of corticogeniculate synapses is formed early and is not altered during subsequent development. Quantitatively, there is no significant change in the size of corticogeniculate terminals or their synaptic vesicles in kittens 2 weeks of age (the youngest measured) and older. In contrast, the synaptic contact lengths of these terminals decreases about 28% between 2 and 12 weeks. During this same period there is approximately a twofold increase in the density of corticogeniculate terminals in the neuropil of lamina A. Since the volume of neuropil in lamina A increases almost fourfold between 2 and 12 weeks, the doubling of corticogeniculate terminal density represents about an eightfold increase in terminal number. After 12 weeks there is little change in the length, density, or number of corticogeniculate synaptic contacts, which suggests that the morphological development of the corticogeniculate pathway is essentially complete by this age.

Aging↗
PubMed1987

Synaptic reorganization in the dorsal lateral geniculate nucleus following damage to visual cortex in newborn or adult cats.

We have studied the effects of making large lesions of visual cortex on the synaptic organization of the dorsal lateral geniculate nucleus (LGN) in the cat. Visual cortex was removed at birth in one group of cats and during adulthood in a second group. Following survival periods of 6 months to 2 years, the organization of synapses made by afferents from the retina in the LGN was investigated quantitatively with the electron microscope. In single thin sections we determined the percentage of retinal axon terminals that made synapses in the LGN, the average number of synapses made by each retinal axon terminal, and the identity of each postsynaptic process. These measurements were made separately for retinogeniculate connections in the A and C laminae of the LGN. For comparison, similar sets of measurements were made in adult cats that had been reared normally. When single thin sections from the A or C laminae of the LGN in normal cats are examined, about 60% of the axon terminals from the retina are seen to make at least one synaptic contact. These contacts can be with dendrites or F profiles or both. On average, each retinogeniculate terminal makes approximately 1.4 synapses in the plane of a single section and contacts dendrites three times as often as F profiles. In the A laminae of the LGN in cats that received a visual cortex lesion at birth or in adulthood, the percentage of retinal terminals that make synapses is the same as in normal cats. Similarly, the average number of synaptic contacts made by each retinogeniculate terminal is not changed by a lesion of visual cortex. In contrast, the number of contacts made with dendrites is reduced markedly, by about 29% after a lesion at birth and 53% after a lesion as an adult. However, these reductions are offset by compensatory increases in the number of contacts made with F profiles, and thus the mean number of contacts made by each retinogeniculate terminal is stabilized at a normal value. In the C laminae of the LGN, retinogeniculate terminals also reapportion their synaptic contacts. In cats with a lesion during adulthood, the redistribution of synapses is compensatory, as in the A laminae. When a lesion is made at birth, however, the number of new retinal contacts made with F profiles exceeds the number of dendritic contacts that are lost. As a result, each retinogeniculate terminal makes about 26% more synapses, in total, than normal.(ABSTRACT TRUNCATED AT 400 WORDS)

Age Factors↗
PubMed1987

Effects of corpus callosum section on functional compensation in the posteromedial lateral suprasylvian visual area after early visual cortex damage in cats.

A visual cortex lesion made in adult cats leads to a loss of direction selectivity and a loss of response to the ipsilateral eye among cells in posteromedial lateral suprasylvian (PMLS) cortex of cats. However, a visual cortex lesion made in young cats results in normal direction selectivity and normal ocular dominance in PMLS cortex. Thus cats with an early lesion demonstrate functional compensation in PMLS cortex. The present experiment determined whether the functional compensation depends upon an intact corpus callosum. Cats received a unilateral visual cortex lesion on the day of birth (day 1) or at 8 weeks of age. When the cats were adult, the corpus callosum was sectioned and 24 hours later recordings were made in PMLS cortex ipsilateral to the visual cortex lesion. Results were compared to cats with a similar lesion and an intact corpus callosum. In cats with a lesion made on day 1, a corpus callosum section did not affect receptive-field properties or ocular dominance in PMLS cortex. Therefore, functional compensation is not dependent on input via the corpus callosum in these animals. However, in cats with a lesion made at 8 weeks. a corpus callosum section resulted in a decrease in the percentage of direction-selective cells and in the percentage of cells driven by the ipsilateral eye. Despite the decrease, the percentage of direction-selective cells still was greater than in cats with an adult unilateral visual cortex lesion. Thus, while partly dependent on callosal inputs, some functional compensation for direction selectivity remains on the basis of ipsilateral inputs.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1986

Genesis of interneurons in the dorsal lateral geniculate nucleus of the cat.

Most neurons in the A-laminae of the cat's dorsal lateral geniculate nucleus (LGN) are born between embryonic days 22 and 32. Whereas approximately 78% of these cells are destined to become geniculocortical relay cells, the remaining 22% of LGN neurons do not appear to establish connections with visual cortex, and therefore can be considered interneurons. In the present study we have combined the 3H-thymidine method for labeling dividing neurons with the retrograde horseradish peroxidase (HRP) method for identifying LGN relay cells in order to study specifically the genesis of interneurons in the cat's LGN. Developing LGN interneurons in 12 kittens were labeled with 3H-thymidine by injecting the radioactive label into the allantoic cavity of their pregnant mothers on different embryonic days. Approximately 8-22 weeks after birth LGN relay cells in the A-laminae were labeled retrogradely by injecting large volumes of HRP into visual cortex areas 17 and 18. LGN cells that could not be labeled retrogradely with HRP were considered to be interneurons. Our results show that interneurons are born on each of the embryonic days studied, E24-E30. This period represents approximately the middle two-thirds of the entire period of LGN neurogenesis. Although the birth rate for interneurons is not uniform, there is no indication from our data that interneurons and relay cells in the cat's LGN are born at different times during LGN neurogenesis.

Animals↗
PubMed1982

Thalamic projections to visual areas of the middle suprasylvian sulcus in the cat.

The thalamic afferents to two areas of the lateral suprasylvian visual cortex in the cat were studied by using retrograde transport of horseradish peroxidase (HRP). Injections were localized retinotopically with electrophysiological recording. The posteromedial lateral suprasylvian area (PMLS) of Palmer et al. ('78) receives afferents from the pulvinar (P), the posterior nucleus of Rioch (PN), the C-laminae of the lateral geniculate nucleus (LGNd) and the centrolateral (CL), lateral posterior (LP), medial interlaminar (MIN) nuclei. The anteromedial lateral suprasylvian area (AMLS) receives afferents from CL, P, LP, PN, MIN, and probably from the posterior nuclear group (PO), and the lateral dorsal (LD) and ventral anterior (VA) nuclei. The LP-pulvinar complex has been divided into four zones on the basis of connectivity: geniculate wing, pulvinar, the lateral division of LP, and the interjacent division of LP (Updyke, '77; Graybiel and Berson, '80; Guillery et al., '80). The locations of labeled cells in the present experiments suggest that both AMLS and PMLS receive afferents from each of the four zones, although differences exist in the strength of the projections. While AMLS and PMLS receive afferents from many of the same nuclei (CL, P, LP, PN, and MIN), differences in their afferents also were noted. These differences are of three types. The first is that some nuclei project to only one of the cortical areas. PMLS alone receives input from the C-laminae of the LGNd while AMLS alone receives probable input from PO, LD, and VA. The second difference is in the strength of the projection from some nuclei. AMLS receives a stronger projection from CL and P than does PMLS. The third difference concerns the pattern of distribution of neurons that project to each cortical area. Labeled cells in LP are dispersed after an AMLS injection, but are found in clusters or bands after a PMLS injection. Thus our results indicate that the thalamic afferents to AMLS and PMLS are in general similar: however, differences in input to AMLS and PMLS suggest that inputs to PMLS are predominantly visual while AMLS receives a broader spectrum of afferent information.

Animals↗
PubMed1971

Anomalous retinal pathways in the Siamese cat: an inadequate substrate for normal bioncular vision.

All major retinal pathways in the Siamese cat are abnormal, with almost total crossing of the projections to the pretectum and superior colliculus. These projections represent a marked disruption in the customary neural substrate for binocular vision, which implies a consequent impairment in stereoscopic depth perception. Crossed eyes, commonly seen in the Siamese cat, may therefore arise from a neuroanatomical defect in the primary visual pathways.

Animals↗