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At least 19 recordsLinked to original sources
PubMed1982

Covariation of distributions of callosal cell bodies and callosal axon terminals in layer III of cat primary auditory cortex.

Primary auditory cortex in the cat is both the source and target of callosal fibers. Injection of horseradish peroxidase (HRP) in the high frequency representation of AI in one hemisphere retrogradely labels callosal cell bodies and anterogradely labels callosal axon terminals in AI of the opposite hemisphere. In tissue sections cut through layer III parallel to the cortical surface, elongated patches composed of dense aggregates of callosal cell bodies and callosal axon terminals alternate with regions containing lower concentrations of these elements. Labeling in AI is most dense in regions corresponding to the frequency representation of the injected site. In layer III of the densely labeled region, patches of high concentrations of labeled callosal axon terminals correspond with high concentrations of labeled callosal cell bodies. On the other hand, little correspondence is apparent between the distributions of the two elements in layer III in the surrounding area of lighter labeling. Layers V and VI contain relatively few labeled callosal axon terminals and cell bodies, and our data do not suggest whether the two distributions covary in these layers.

Afferent Pathways↗
PubMed2003

An Arabidopsis Callose Synthase, GSL5, Is Required for Wound and Papillary Callose Formation.

Arabidopsis was transformed with double-stranded RNA interference (dsRNAi) constructs designed to silence three putative callose synthase genes: GLUCAN SYNTHASE-LIKE5 (GSL5), GSL6, and GSL11. Both wound callose and papillary callose were absent in lines transformed with GSL5 dsRNAi and in a corresponding sequence-indexed GSL5 T-DNA insertion line but were unaffected in GSL6 and GSL11 dsRNAi lines. These data provide strong genetic evidence that the GSL genes of higher plants encode proteins that are essential for callose formation. Deposition of callosic plugs, or papillae, at sites of fungal penetration is a widely recognized early response of host plants to microbial attack and has been implicated in impeding entry of the fungus. Depletion of callose from papillae in gsl5 plants marginally enhanced the penetration of the grass powdery mildew fungus Blumeria graminis on the nonhost Arabidopsis. Paradoxically, the absence of callose in papillae or haustorial complexes correlated with the effective growth cessation of several normally virulent powdery mildew species and of Peronospora parasitica.

Arabidopsis↗
PubMed1993

Stimulation of Callose Synthesis in Vivo Correlates with Changes in Intracellular Distribution of the Callose Synthase Activator [beta]-Furfuryl-[beta]-Glucoside.

[beta]-Furfuryl-[beta]-glucoside (FG) has been shown to be a specific endogenous activator of higher plant callose synthase (P. Ohana, D.P. Delmer, G. Volman, J.C. Steffens, D.E. Matthews, M. Benziman [1992] Plant Physiol 98: 708-715). Because glycosides such as FG are usually sequestered in vacuoles, we have proposed that activation of callose synthesis in vivo may involve a change in the compartmentation of FG and Ca2+, resulting in a synergistic activation of callose synthase. The use of suspension-cultured barley (Hordeum bulbosum L.) cells provides evidence that FG is largely sequestered in the vacuole. Furthermore, conditions that lead to induction of callose synthesis in vivo correspondingly lead to elevation of the cytoplasmic concentration of FG. These conditions include the lowering of cytoplasmic pH or elevation of cytoplasmic Ca2+. Oligogalacturonide elicitors have also been reported to cause similar changes in cytoplasmic pH and Ca2+ concentration (Y. Mathieu, A. Kurkdjian, H. Xia, J. Guern, A. Koller, M.D. Spiro, M. O'Neill, P. Albersheim, A. Darvill [1991] The Plant Journal 1: 333-343), and such an elicitor also causes an elevation in cytoplasmic FG coupled with stimulation of callose synthesis. These results support the concept that a relative redistribution of FG between cytoplasm and vacuole may be one of the components of the signal transduction pathway for elicitation of callose synthase in vivo.

Journal Article↗
PubMed1995

Extent and limits of callosal plasticity: presence of disconnection symptoms in callosal agenesis.

Although earlier studies have emphasized the absence of 'split-brain' symptoms in callosal agenesis patients, the notion of an 'asymptomatic' acallosal brain has lately been challenged. We report a number of findings that are indicative of an interruption of interhemispheric communication and integration in individuals lacking the corpus callosum. Several groups of patients with callosal pathology (acallosals, patients with commissurotomy or callosotomy, either complete or partial) were compared to matched controls. Interhemispheric transfer was tested in two different experiments involving pointing to a light source while maintaining central fixation. In the first experiment, a learning paradigm was used to measure transfer of a motor skill from the trained to the untrained hand. In the second experiment, subjects pointed to visual targets at different locations on a perimeter. Midline fusion, a recurrent theme when describing callosal function, was assessed using tasks which included depth perception with binocular and/or monocular cues, two-point discrimination thresholds and sound localization in the peri-central and lateral fields. Subjects with callosal pathology were impaired on all tasks involving transfer of motor and visuo-spatial skills and on some of the tasks requiring sensory integration of visual and tactile information across the body midline. We conclude that these functions require an intact corpus callosum since none of these deficits were seen in controls equated for IQ.

Adolescent↗
PubMed1984

Termination of callosal afferents onto identified callosal projection neurons in the primary motor cortex of the mouse.

Techniques utilizing the retrograde transport of horseradish peroxidase and lesion-induced degeneration have been used to identify neurons which form the callosal projection pathway and callosal axon terminals in the primary motor cortex of the mouse. Synapses occur between callosal projection neurons and degenerating callosal afferents, demonstrating a direct synaptic link between neurons which project to homotopic regions of the contralateral cortex.

Animals↗
PubMed2000

[A case of callosal apraxia without agraphia and acquired stuttering associated with callosal infarction].

We report a 52-year-old right-handed man with cerebral infarction of the right anterior cerebral artery area. The MRI findings showed cerebral infarction in the trunk of the right corpus callosum, although some part of the posterior half of the trunk was spared. Some part of right precuneal gyrus, cingulate gyrus were also involved. The clinical feature of this case is characterized by following two points. First, although callosal apraxia is usually accompanied by agraphia, he showed apraxia with the left hand, but showed no agraphia. Secondary, he showed speech dysfluency mainly characterized by initial syllable repetitions. The nature of this speech dysfluency was determined as acquired stuttering. This case suggests that the pathway for praxis locates distinct portion from that for writing on corpus callosum. We analyzed callosal lesions of previous studies reporting callosal apraxia without agraphia, then compared to that of this case. And we also reviewed acquired stuttering report caused by callosal lesions. Consequently, we suggest that apraxia and stuttering were caused by damage of the trunk of the corpus callosum. While writing was preserved by the intact fibers in the posterior half of the trunk.

Apraxias↗
PubMed1991

Neurons with callosal projections in visual areas of newborn kittens: an analysis of their dendritic phenotype with respect to the fate of the callosal axon and of its target.

Combined retrograde transport of Rhodamine-labeled latex beads and intracellular injection of Lucifer Yellow in aldehyde-fixed slices of areas 17 and 18 in kittens indicate that neurons with similar dendritic morphology send axons into the corpus callosum from the 17/18 border and from parts of area 17 destined to become acallosal. At both sites callosally projecting neurons (callosal neurons) include pyramids, spiny stellate cells and star-pyramids; two types of pyramidal neurons can be distinguished on the basis of the complexity of their apical dendrites. At both sites, the dendritic morphology of callosal neurons appears basically unaffected by the ablation at the beginning of the second postnatal week of the contralateral areas 17 and 18 to which they have sent their axon. Thus the dendritic morphology of this type of cortical neuron seems independent of retrograde signals coming from their contralateral target and may instead depend on "programs" intrinsic to the neurons and/or conditions acting locally on their cell bodies, dendrites or initial axon collaterals.

Animals↗
PubMed1985

The callosal system of the superior parietal lobule in the monkey.

The callosal connections of the superior parietal lobule, area 5 of Brodmann, were studied in macaque monkeys (M. nemestrina and M. fascicularis) using anatomical techniques based on both anterograde and retrograde axoplasmic transport of wheat-germ-agglutinin-conjugated horseradish peroxidase. From sagittal sections, two-dimensional flattened computer reconstructions of the volumes of cortical tissue containing callosal-projecting neurons (callosal efferent zone) and/or callosal terminal axons (callosal terminal territory) were obtained. Callosal zones were found in area 5, including the supplementary sensory area, in a limited part of area 6, i.e., in the supplementary motor area, in area 7b, in the cortex of the dorsal bank of the sylvian fissure, and in a limited part of area 7a, in the cortex of the upper third of the rostral bank of the superior temporal sulcus. Callosal neurons in all cortical areas studied, though with regional variations, predominated in layer IIIb, but were also very numerous in layers VI and V. They were rare in other cortical laminae. In the cortical regions projecting heterotopically to area 5, the tangential distribution of callosal neurons was discontinuous because of the presence of large acallosal regions. These were not observed in area 5, although here the distribution of callosal neurons waxed and waned in the tangential cortical plane. Callosal axons to and/or from area 5 crossed the midline in the posterior, presplenial part of the corpus callosum. In the superior parietal lobule they terminated in radial patches or columns, spanning layers I-IV. These columns of various width (200-2,000 micron) were separated by gaps of similar size, free of such terminals. Callosal neurons were present not only within, but also between, the callosal terminal columns. Callosal neurons located within the callosal terminal columns were, in a statistically significant way, more numerous than those located between them. The callosal efferent zone occupied 71% of the tangential domain of area 5, whereas the callosal terminal territory occupied only 49% of it. This difference is statistically significant. The discontinuous columnar arrangement of callosal terminals and the periodic distribution of callosal neurons in the lateral part of area 5 defined three main bands of callosal connections of irregular shape which were oriented mediolaterally and ran parallel to the main architectonic borders, the border between areas 2 and 5 and that between 5 and 7.

Animals↗
PubMed1987

Development of visual callosal connections in neonatally enucleated rats.

The present report extends previous descriptions of the mature distributions of callosal cells and axonal terminations in rats monocularly or binocularly enucleated at birth. It also describes the time course of callosal development in these animals, and establishes the age at which eye removal ceases to alter the normal course of callosal development. Although our results indicate that the callosal pattern is anomalous in adult, neonatally enucleated rats, the major features of the normal callosal pattern are nonetheless clearly recognizable in both monocularly and binocularly enucleated rats. Thus, as in normally reared rats, there are dense accumulations of callosal cells and terminations at the 17/18a border region, at the lateral border of area 18a, and within area 18b in enucleated rats. In addition, several narrow bands of callosal connections bridge the width of area 18a at several rostrocaudal levels, and a ring-like callosal configuration is located anterolateral to area 17. In monocularly enucleated rats, the most prominent anomaly develops in the hemisphere ipsilateral to the remaining eye, where a dense band of callosal connections runs rostrocaudally through the center of area 17. Periodic fluctuations in the density of labeling along the length of this extra band give it a beaded appearance. The callosal pattern in the hemisphere contralateral to the remaining eye in these rats appears normal. Binocular enucleation causes the appearance of discrete regions of reduced labeling within the 17/18a callosal band and several densely labeled tongue-like regions that extend medially from this band well into area 17. The laminar distribution of callosal cells and terminations is not significantly altered by loss of one or both eyes at birth. Our data indicate that enucleation does not affect the time course of callosal development. Thus, in enucleated pups, all features of the mature callosal pattern can be recognized by 6-7 days of age, and by 12 days of age the patterns appear virtually mature. Finally, our data reveal that monocular or binocular enucleations performed at 6 days of age or later allow the callosal pattern to develop normally, whereas enucleations performed between birth and 5 days of age produce anomalies similar to those observed in rats enucleated at birth. Thus, at about 6 days of age--just as the earliest features of the mature callosal pattern become discernible, and long before rats first open their eyes--the developing callosal pathway is no longer susceptible to disruptions of visual input.

Age Factors↗
PubMed1992

Development of callosal connections in the sensorimotor cortex of the hamster.

To investigate the development of corpus callosal connectivity in the hamster sensorimotor cortex, we have used the sensitive axonal tracer 1,1 dioctadecyl-3,3,3',3', tetramethylindocarbocyanine perchlorate (DiI), which was injected either in vivo or in fixed brains of animals 3-6 days postnatal. First, to study changes in the overall distribution of developing callosal afferents we made large injections of DiI into the corpus callosal tract. We found that the anterogradely labeled callosal axons formed a patchy distribution in the contralateral sensorimotor cortex, which was similar to the pattern of adult connectivity described in earlier studies of the rodent corpus callosum. This result stands in contrast to previous retrograde studies of developing callosal connectivity which showed that the distribution of callosal neurons early in development is homogeneous and that the mature, patchy distribution arises later, primarily as a result of the retraction of exuberant axons. The initial patchy distribution of callosal axon growth into the sensorimotor cortex described in the present study suggests that exuberant axons destined to be eliminated do not enter the cortex. In addition, small injections of DiI into developing cortex resulted in homotopic patterns of callosal topography in which reciprocal regions of sensorimotor cortex are connected, as has been shown in the adult. Second, to study the radial growth of callosal afferents we followed the extension of individual callosal axons into the developing cortex. We found that callosal axons began to invade the contralateral cortex on about postnatal day 3, with little or no waiting period in the callosal tract. Callosal afferents then advanced steadily through the cortex, never actually invading the cortical plate but extending into layers on the first day that they could be distinguished from the cortical plate. The majority of callosal axons grew radially through the cortex and did not exhibit substantial branching until postnatal day 8, the age when the cortical plate disappears and callosal afferents reach the outer layer of cortex. This mode of radial growth through cortex prior to axon branching could serve to align callosal afferents with their radial or columnar targets before arborizing laterally.

Anesthesia↗
PubMed1985

Organization and postnatal development of callosal connections in the visual cortex of the rat.

The distribution of callosal cells and terminals was studied in the posterior neocortex of pups whose ages ranged from 3 to 16 days and in adult rats 2 months of age or older. Callosal cells and terminations were revealed using retrograde (horseradish peroxidase) and anterograde (horseradish peroxidase; tritiated proline) tracing techniques, respectively, and the distribution of callosal connections was analyzed in tangential or coronal histological sections. In agreement with previous studies, we observed that the pattern of callosal connections in areas 17 and 18 of adult rats contains the following features: (1) a dense band of callosal cells and terminations separating the interiors of areas 17 and 18a, (2) a ringlike configuration anterolateral to area 17, (3) a region of dense labeling lateral to area 18a, (4) several narrow bands of labeling that bridge area 18a at different anteroposterior levels, and (5) one or more labeled regions in area 18b. In all these callosal regions, labeled cells and terminations are densely aggregated in layers II-III, Va, and Vc-VIa, and less densely in layer IV and the remaining portions of layers V and VI. High densities of isotope-labeled fibers are also observed in the lower half of layer I. Throughout the interiors of areas 17 and 18a, a significant number of labeled cells are observed in layers Vc-VIa. In contrast to adult rats, in neonates no distinct tangential pattern of callosal connections is apparent. Instead, labeled cells are densely aggregated in two continuous horizontal bands located in cortical layers Va and Vc-VIa, and callosal axons are largely restricted to white matter. During the first 2 postnatal weeks there is a progressive loss of callosal cells in regions that normally have few callosal cells in the adult (e.g., interiors of areas 17 and 18a) and an increase in the number of cells in layers II-IV in regions that are densely callosal in the adult (e.g., callosal regions at the 17/18a border, lateral border of area 18a, and in area 18b). The decrease in the number of callosal cells in the interiors of areas 17 and 18a is more severe in the upper than in the lower band of the immature labeling pattern, and our data from tangential sections indicate that this loss of callosal neurons occurs synchronously across the interiors of these areas. During this period there is also a localized invasion of labeled callosal axons into those regions of gray matter where they will be found in adult life.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1986

Synaptic connections of callosal projection neurons in the vibrissal region of mouse primary motor cortex: an electron microscopic/horseradish peroxidase study.

Reciprocal axonal projections between homotypic areas of the vibrissal region of mouse primary motor cortex (MsI) (Porter and White: Neurosci. Lett. 47:37-40, '84) suggested the existence of reciprocal synaptic connections between callosal projection neurons and callosal afferents. In the present study, the retrograde transport of horseradish peroxidase (HRP) was combined with lesion-induced degeneration to identify synapses between callosal afferents and callosal neurons in the corresponding region of the contralateral cortex. The procedure was as follows: MsI was injected with HRP and aspirated on the following day. After 4 days, the animals were perfused and motor cortex was processed for HRP according to a variation of the Adams (Brain Res. 176:33-47,'77) technique, and postfixed in OsO4. The methods used consistently filled fine dendritic branches and spines with dense reaction product, thus allowing examination of synaptic contacts with these processes. All callosal projection neurons were identified as pyramidal neurons, having somata in cortical layers II/III and V. Labeled cells from each of the two levels were prepared for electron microscopy, and that part of each cell's apical dendrite that traversed the superficial cortical layers, where most callosal axons terminate, was cut in an unbroken series of thin sections. Micrographs were taken of all labeled profiles in each thin section, and tracings of the profiles were assembled to reconstruct the apical dendrites. Data on the distribution, type, and amount of callosal and other synapses with the shaft and spines of the apical dendrites were obtained by examining the reconstructions. In addition, profiles of basal dendrites of layer II/III cells were examined in thin sections to ascertain the numbers of callosal and other synapses formed with their shafts and spines. The proportion of synapses that each dendrite formed with callosal axon terminals was compared to the concentration of callosal afferents in the neuropil. Dendrites of both layer II/III and layer V pyramidal cells synapsed with callosal axon terminals. The apical and basal dendrites of layer II/III neurons formed a similar proportion of their synapses with callosal afferents, and this was similar to the concentration of callosal synapses in the surrounding neuropil. Segments of apical dendrites belonging to layer V and layer II/III neurons course through neuropil containing nearly the same concentration of degenerating callosal terminals, but the layer V cells form fewer callosal synapses.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1988

Topography of interhemispheric connections in neocortex of mice with congenital deficiencies of the callosal commissure.

Normally, axons within the corpus callosum are ordered according to the cortical regions from which they originate, and callosal cells and terminations form elaborate cortical patterns related to the underlying topographic representations of the sensory periphery. About 30% of mice of the BALB/c strain show congenital deficiencies of the callosal commissure which range from total absence of the corpus callosum to a moderate reduction in the size of this commissure. In the light of current theories about the origin of these callosal deficiencies, it seems likely that fibers crossing the midplane in mutant mice have to circumvent local disturbances along their migration path. Since these disturbances in fiber trajectory may, in turn, alter the overall pattern of callosal projections, we set out to investigate whether the distribution of callosal connections in mice with marked deficiencies of the corpus callosum is as ordered as in normal mice. In groups of normal and mutant mice, we used multiple injections of horseradish peroxidase to reveal the overall distribution of callosal connections and restricted injections of horseradish peroxidase conjugated with wheat germ agglutinin to reveal finer aspects of the organization of the callosal pathway in these animals. Our results show that the number of labeled cells is reduced in mice with a small corpus callosum and that no labeled cells are present in the neocortex of acallosal mice. Furthermore, the topographic distribution of fibers within the corpus callosum of mutant mice can be significantly less ordered than in normal mice. However, even in mice with extreme deficiencies of the corpus callosum, callosal fibers originate from and terminate in all major areas of the cortex, and, within these areas, callosal cells and terminations are distributed according to the normal plan. The laminar distribution of callosal cells also appears normal in these mice. These findings indicate that gross developmental anomalies of the corpus callosum do not prevent normal specification of the callosal pattern during development. Within the context of current theories about the origin of congenital callosal deficiencies, our findings suggest that callosal fibers are able to establish appropriate contralateral connections in spite of alterations of their migration route. They also suggest that fiber topography within the corpus callosum does not play an important role in guiding migrating axons to their correct contralateral targets. Finally, our failure to find labeled fibers within the anterior commissure indicates that this commissure does not serve as an alternative route for deviated callosal axons.

Agenesis of Corpus Callosum↗