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G Leuba

Publications and source records attributed to G Leuba.

33 records · Page 2Linked to original sources
PubMed1984

Development of dendritic patterns in the lateral geniculate nucleus of monkey: a quantitative Golgi study.

Quantitative analysis of dendritic branching patterns was performed in rapid Golgi sections of the lateral geniculate nucleus of Old World monkeys at several ages, using a computer-microscope and a tree-analysing program. In parvocellular and magnocellular multipolar neurons the dendrites were analysed in centrifugal order and according to whether they were intermediate or terminal segments. Between late gestation and birth there is an increase in the mean length of dendrites, and in the total length of dendrites per neuron, more pronounced in magnocellular layers; there follows a progressive decrease in their length until adulthood. However, only terminal dendritic segments are involved in these changes in length. Intermediate segments are shorter and show a more or less constant length throughout life. The final length of a segment seems more determined by it being terminal or intermediate than by its order of branching and there is greater plasticity in the terminal part of the dendritic tree. Magnocellular neurons are characterized by a greater number of both intermediate and terminal segments than parvocellular neurons but not by a greater length of individual segments. This accounts for the greater dendritic length in magnocellular neurons and may offer them a larger surface for synaptic connectivity.

Animals↗
PubMed1979

Long-term effects of postnatal undernutrition and maternal malnutrition on mouse cerebral cortex. I. Cellular densities, cortical volume and total numbers of cells.

Quantitative analysis of cellular densities as well as an estimate of the cortical volume and of its total cell population were performed on the cortex of postnatally undernourished mice (2--21 days) and on that of pups from malnourished mothers (gestation and lactation). Animals were followed until 180 days of age after more than 5 months of nutritional rehabilitation, and data were obtained at 10, 30, 60, and 180 days of age. The neuronal density was much higher in all cortical layers of the two experimental series, suggesting a delay in cortical maturation. Moreover, layers II, III, and IV were more delayed than layers I, V, and VI. Postnatal undernutrition had more severe effects than maternal malnutrition and the degree of recovery after a long rehabilitation was much less. The increase of the cortical volume was greatly reduced in postnatal undernutrition and to a lesser degree in maternal malnutrition. The total number of glial cells was also reduced more in postnatal undernutrition than in maternal malnutrition, but the total number of neurons was never smaller than in the controls.

Age Factors↗
PubMed1979

Long-term effects of postnatal undernutrition and maternal malnutrition on mouse cerebral cortex. II. Evolution of dendritic branchings and spines in the visual region.

Quantitative analysis of the dendritic branchings of pyramidal cells from layers V and III, as well as of the number of spines on their apical dendrites, were performed on the visual cortex of postnatally undernourished mice (2nd--21st day) and on that of pups from malnourished mothers (gestation and lactation). Animals were followed till 180 days of age after more than 5 months of nutritional rehabilitation, and data were obtained at 10, 15, 21, 30, 60, and 180 days of age. The increase and maturation of dendritic branchings and spines were much more reduced in postnatal undernutrition than in maternal malnutrition. Furthermore, permanent damage still remained at 180 days in postnatal undernutrition while almost no damage was statistically detectable after maternal malnutrition.

Age Factors↗
PubMed1978

Postnatal development of the mouse cerebral neocortex. III. Some dynamical aspects.

In this paper we analyse our data from the quantitative cytoarchitectonic study of motor and sensory areas 10--4--3 and 2(Leuba and coll., 1977) and of visual and auditory area 5--17--18a--18--41 and 20 (Heumann and coll., 1977). The analysis of neuronal densities and cortical depths shows the following facts during the postnatal maturation: 1. Generally the sequence of maturation of the cortical layers is the same in the 9 studied areas: first layers I. and V, then VIb and VIa followed by III and IV and finally II. 2. This sequence is the same between 5 and 10 days as between 10 and 30 days. Still the maturation is much faster between 5 and 10 days. After 30 day differences between the layers are not very important. 3. For layers I, V and VI our 9 areas show an approximately similar degree of development from 5 days on. 4. Layers II, III and IV are in a faster period of development between 5 and 10 days. At this moment and for these layers, areas 17, 2, 3, 4 and 10 are less well developed than areas 41, 20, 18 and 18a. 5. One can thus consider that in mice the maturation of the areas seems to be more correlated with their localization than with their function. Effectively areas 41, 20 and 18a are in the vicinity of the rhinal fissure and a maturational gradient may start in this fissure. 6. In terms of neuronal densities and cortical depths an adult aspect of the layers and of the areas seems to be reached around 30 days. But some other phenomena of maturation exist after 30 days.

Aging↗
PubMed1978

Postnatal development of the mouse cerebral neocortex. IV. Evolution of the total cortical volume, of the population of neurons and glial cells.

The total neocortical volume delimited between precise anatomical features was measured. Serial frontal sections cresyl-violet stained were measured with plainimetric methods and the total volume evaluated at 5, 10, 30, 60 and 180 days. The total volume was used to obtain the total number of neurons and glial cells at each age using our quantitative data (published in our previous papers). The evolution of the cellular densities were studied in the sensory and motor areas 10--4--3 and 2 (Leuba and coll. 1977) and in the visual and auditory areas 17--18a--18--41 and 20 (Heumann anc coll. 1977) in the mouse cerebral neocortex. 1. The total neocortical volume increases rapidly between 5 and 10 days, less between 10 and 30 days, slightly decreases at 60 days and reincreases at 180 days. 2. Between 5 and 30 days, the loss of cortical neurons is of about 30% by neuronal death. 3. The total number of glial cells doubles between 5 and 180 days. The increase is progressive through the development.

Animals↗
PubMed1977

Postnatal development of the mouse cerebral neocortex. I. Quantitative cytoarchitectonics of some motor and sensory areas.

Quantitative data have been obtained (numbers of neurons and glial cells in a cube of 0.000 25 mm3, thicknesses of cortical layers, nuclear diameters of neurons) on Cresyl Violet stained sections from the six cortical layers of the Swiss Albinos mouse brain through the postnatal development at 5, 10, 30, 60 and 180 days. 1) Normative data of the cortical cell population are now available from motor areas 4 and 10 and sensory areas 3 and 2 according to KRIEG (1946). The evolution of the neuronal densities through time was obtained and was taken as a criterion of maturation for the different layers in the studied cortical areas. 2) Areas 4, 10, 3 and 2 have been described histologically at all the mentioned ages. 3) The nuclear diameter of the neurons increases in all the layers between 5 and 10 days and less between 10 and 30 days. It remains stable from 30 days on. 4) At adult age the sensory areas 3 and 2 show a greater thickness of the group of supragranular layers II, III and IV than of the infragranular layers V and VI together. Layer V shows the same thickness in areas 2, 3 and 4. The same is true for layer VI in the same areas. In area 10 layers V and VI are thicker than in areas 2, 3 and 4. At younger ages (5 and 10 days) the relative thicknesses of the different layers are of the same order but each layer is thinner. 5) The neuronal density shows the same type of development in the four studied areas. Maturation in terms of decrease of neuronal densities is very rapid between 5 and 10 days and slows down till 30 days with speeds depending on the layers. Layers I, V and VI show faster and earlier maturation than layers II, III and IV. 6) The glial density is mostly stable through the development. This does not mean that there is no glial proliferation. 7) The delineation between the different areas according to KRIEG's (1946) atals and/or CAVINESS's (1975) publication are discussed taking into account our quantitative data.

Animals↗
PubMedDate not supplied

Visual cortex in Alzheimer's disease: occurrence of neuronal death and glial proliferation, and correlation with pathological hallmarks.

Visual areas 17 and 18 were studied with morphometric methods for numbers of neurons, glia, senile plaques (SP), and neurofibrillary tangles (NFT) in 13 cases of Alzheimer's disease (AD) as compared to 11 controls. In AD cases, the mean neuronal density was significantly decreased by about 30% in both areas 17 and 18, while the glial density was increased significantly only in area 17. The volume of area 17 was unchanged in AD cases but its total number of neurons was decreased by 33% and its total number of glia increased by 45% compared to controls. In AD the number of SP was similar in areas 17 and 18, while that of NFT was significantly higher in area 18. The number of neurons with NFT was only 2% in area 17 and about 10% in area 18. The discrepancy between the loss of neurons and the amount of NFT suggests that neuronal loss can occur without passing through NFT degeneration. The deposition of SP was correlated with glial proliferation, but not with neuronal loss or neurofibrillary degeneration.

Aged↗
PubMedDate not supplied

Calcium-binding proteins immunoreactivity in the human subcortical and cortical visual structures.

The distribution of neurons and fibers immunoreactive (ir) to the three calcium-binding proteins parvalbumin (PV), calbindin D-28k (CB), and calretinin (CR) was studied in the human lateral geniculate nucleus (LGN), lateral inferior pulvinar, and optic radiation, and related to that in the visual cortex. In the LGN, PV, CR, and CB immunoreactivity was present in all laminae, slightly stronger in the magnocellular than in the parvocellular laminae for CB and CR. PV-ir puncta, representing transversally cut axons, and CR-ir fibers were revealed within the laminae and interlaminar zones, and just beyond the outer border of lamina 6 in the geniculate capsule. In the optic radiation both PV- and CR-immunoreactive neurons, puncta, and fibers were present. CB immunoreactivity was revealed in neurons of all laminae of the lateral geniculate nucleus, including S lamina and interlaminar zones. There were hardly any CB-ir puncta or fibers in the laminae, interlaminar zones, geniculate capsule, or optic radiation. In the lateral inferior pulvinar, immunoreactive neurons for the three calcium-binding proteins were present in smaller number than in the LGN, as well as PV-ir puncta and CR-ir fibers within the nucleus and in the pulvinar capsule. In the white matter underlying area 17, fibers intermingled with a few scattered neurons were stained for both PV and CR, but very rarely for CB. These fibers stopped at the limit between areas 17 and 18. Area 17 showed a dense plexus of PV-ir puncta and neurons in the thalamo-receptive layer IV and CR-ir puncta and neurons both in the superficial layers I-II, IIIC, and in layer VA. Cajal-Retzius CR-ir neurons were present in layer I. CB-ir puncta were almost confined to layer I-III and CB-ir neurons to layer II. Finally the superior colliculus exhibited mostly populations of PV and CR pyramidal-like immunoreactive neurons, mainly in the intermediate tier. These data suggest that in the visual thalamus most calcium-binding protein immunoreactive neurons project to the visual cortex, while in the superior colliculus a smaller immunoreactive population represent projection neurons.

Adult↗
PubMedDate not supplied

Neuronal death in the development and aging of the cerebral cortex of the mouse.

The numbers of neurons and glial cells in the cerebral cortex of the mouse have been estimated during its whole life-span (5 to 720 days), taking into account both the cellular densities of several areas and the cortical volumes. The results clearly demonstrate that there is a massive neuronal loss in the cerebral cortex during early postnatal development, greater in layers II-IV than in layers V-VI. In contrast, aging is characterized by a discrete neuronal loss in the cerebral cortex, purely restricted to layers II-IV. The number of glial cells increases continuously from 5 to 720 days. We emphasize here the need to obtain volumetric measure together with cellular densities in order to get interpretable quantitative data on cellular death and proliferation.

Aging↗
PubMedDate not supplied

Aging of dendrites in the cerebral cortex of the mouse.

Quantitative analysis of the dendritic branchings of pyramidal cells in layers V and III of the visual cortex was performed in aging mice (540 and 720 days) and compared to adult mice (180 days). The number of spines on apical dendrites of the same cells was also counted. Between 180 and 720 days of age, the decrease in dendritic branchings around the perikaryon was dramatic (30-40%) and that in dendritic spines was even more so (about 50%). However, most of the decrease in both dendritic branchings and spines has already occurred at 540 days, and the difference between 540 and 720 days was not statistically significant. This suggests a real loss in cortical connections with aging, taking place prior to the final months of the lifespan of the mouse.

Aging↗
PubMedDate not supplied

No detected mutations in the genes for the amyloid precursor protein and presenilins 1 and 2 in a swiss early-onset Alzheimer's disease family with a dominant mode of inheritance.

Mutations have been found in more than a hundred early-onset families with Alzheimer's disease (AD) in the genes for the amyloid precursor protein, presenilin 1 and presenilin 2. The object of our investigation was to identify if these mutations or novel ones were operating in a Swiss early-onset AD family (mean age of onset: 53.3 years) with 7 members available, all neuropathologically confirmed. No known or new mutations were detected. Thus, our data support the existence of a yet unknown mutation, or other genes, contributing to familial early-onset AD. CopyrightCopyright 1999S.KargerAG,Basel

Adult↗
PubMedDate not supplied

Mild amyloid pathology in the primary visual system of nonagenarians and centenarians.

In order to study the patterns of Alzheimer disease (AD)-related pathology in the primary visual system of the oldest old, we performed a quantitative analysis of senile plaques (SP), diffuse beta amyloid (A beta) deposit and neurofibrillary tangle (NFT) distribution in primary area 17, and a semi-quantitative analysis in the dorsal lateral geniculate nucleus (LGN), lateral inferior pulvinar (LIP) and superior colliculus (SC) of 21 individuals aged between 93 and 102 years. Among them, 10 cases were considered as non-demented (ND), while 9 presented very mild cognitive impairment (VMCI), and 2 cases had a clinical diagnosis of AD. Silver methenamine and Gallyas staining, A beta and tau immunostaining revealed the distribution of AD lesions. In primary area 17, most cases, either ND or with VMCI displayed a low to medium number of SP. There was no significant difference in SP and A beta deposit densities between ND and VMCI groups. On the whole, 0.4--2.4% of the cross-sectional cortical area was covered with A beta deposits. Only 6 cases, either ND or with VMCI, were totally devoid of SP and diffuse A beta deposits. Among the subcortical structures, the LIP and SC exhibited low densities of SP and A beta deposits in about half of the ND and VMCI cases, while the LGN was totally spared. NFT were almost absent in area 17 and subcortical nuclei of ND and VMCI cases. These data imply that the ageing of the primary visual system in ND and VMCI nonagenarians and centenarians is characterised by the frequent development of mild amyloid pathology in area 17 in the absence of NFT. In agreement with previous studies in very old cohorts, they also suggest that amyloid deposition is not related to the early stages of the dementia process in the oldest old.

Aged↗