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A Schleicher

Publications and source records attributed to A Schleicher.

At least 37 records · Page 2Linked to original sources

Observer-independent method for microstructural parcellation of cerebral cortex: A quantitative approach to cytoarchitectonics.

We describe a new, observer-independent procedure for identifying boundaries between cortical areas. The method is useful for images obtained from sections which provide microstructural information on the cortical laminar pattern, e.g., Nissl-, myelin-, or immunohistochemically stained sections or receptor autoradiographs. The laminar pattern is represented by profile curves extending from the cortical surface to the white matter boundary. These profiles are constructed from digitized images. Digitization is based on the grey level index (Nissl) or densitometry (myelin, immunohistochemistry, receptor autoradiography). The shapes of neighboring profiles are compared by calculating their distances according to feature vectors extracted from the profiles. Profiles derived from a homogeneous area can be expected to be similar in shape and hence show low distance values between each other. Maximum distances can be found between profiles which lie on opposite sides of a structural boundary. The Mahalanobis distance was found to be more sensitive and to yield greater spatial resolution than other distance measures such as the Euclidean distance. Cell-stained sections of the human neocortex were analyzed. The method not only verified boundaries which had been defined by visual inspection, it also revealed new ones which had not been detected visually. The procedure offers an important supplement to the traditional methods based on visual inspection which, for the first time, is based on quantitative data and therefore offers a new level of reproducibility and observer independence. Anatomical atlases based on this procedure thus provide a new tool for the interpretation of structural data obtained from functional imaging techniques.

Brain Mapping↗

Areas 3a, 3b, and 1 of human primary somatosensory cortex.

This study defines cytoarchitectonic areas 3a, 3b, and 1 of the human primary somatosensory cortex by objective delineation of cytoarchitectonic borders and ensuing cytoarchitectonic classification. This avoids subjective evaluation of microstructural differences which has so far been the only way to structurally define cortical areas. Ten brains were fixed in formalin or Bodian's fixative, embedded in paraffin, sectioned as a whole in the coronal plane at 20 microm, and cell stained. Cell bodies were segmented from the background by adaptive thresholding. Equidistant density profiles (125 microm wide, spacing 300 or 150 microm) were extracted perpendicularly to the pial surface across cortical layers II-VI and processed with multivariate statistical procedures. Positions of significant differences in shape between adjacent groups of profiles were correlated with the cytoarchitectonic pattern. Statistically significant borders can be reproduced at corresponding positions across a series of nearby sections. They match visible changes in cytoarchitecture in the cell-stained sections. Area 3a lies in the fundus of the central sulcus, and area 3b in the rostral bank of the postcentral gyrus. Area 1 lies on its crown and reaches down into the postcentral sulcus. Interareal borders, however, do not match macrostructural landmarks of the postcentral gyrus, and they considerably vary in their positions relative to these landmarks across different brains. Hence, only genuine microstructural analysis can define the borders between these cortical areas. Additional significant borders which do not correlate with visible changes in cytoarchitecture can be found within areas 3b and 1. They may represent somatotopy and/or cortical representations of different somatosensory receptors.

Adult↗

Mapping of histologically identified long fiber tracts in human cerebral hemispheres to the MRI volume of a reference brain: position and spatial variability of the optic radiation.

The interpretation of the anatomical basis of functional deficits after subcortical infarcts could be considerably improved, if the precise topography and interindividual variability in size and course of long fiber tracts in adult human cerebral hemispheres were available in a spatial reference system. We therefore developed a method enabling the mapping of long fiber tracts to the volume of a standard reference brain. The examined fiber tracts were identified in myelin-stained histological serial sections of 10 human brains. The reference brain is a 3-D reconstruction of in vivo obtained magnetic resonance images (MRIs). The warping of histological volumes with the labeled fiber tracts to the reference brain by means of linear and nonlinear transformation procedures results in population maps that demonstrate the interindividual variability in position, size, and course of fiber tracts. In this paper, we present population maps of the optic radiation and the lateral geniculate body as a first example of this mapping strategy. Both structures present a considerable interindividual variability. Furthermore, voxel-based morphometry shows significant side differences with larger volumes of both structures in the left hemisphere than in the right hemisphere. A more than twofold variability of size in the interhemispheric extension of the optic radiation and the lateral geniculate body is found even after normalization of absolute brain size. Our observations demonstrate that the present approach based on population maps of fiber tracts and nuclei can improve the anatomical localization and interpretation of brain lesions visible in MRIs at the level of microstructurally identified architectonical units.

Adult↗

Different nitric oxide synthase inhibitors cause rapid and differential alterations in the ligand-binding capacity of transmitter receptors in the rat cerebral cortex.

Inhibitors of nitric oxide (NO) synthesis reduce postlesional neuronal death during reperfusion injury by reducing the NO-mediated increase in excitatory neurotransmitter-release. The protective effects of various NO-synthase (NOS) inhibitors differ due to their isoform selectivity. The effects of NO-mediated excessive neurotransmitter supply are transmitted via specific neurotransmitter receptors expressed by the target cells. We report changes in the ligand-binding of different excitatory and inhibitory neurotransmitter-receptors studied by in vitro receptor autoradiography after in vivo-application of NOS-inhibitors. Since the constitutively expressed neuronal NOS-I is area-specifically distributed within the rat cortex, numerous cortical areas were studied in non-lesioned rats, in order to analyze the area-specific effects of NOS-inhibitors. The results showed that the NOS-I-specific inhibitor 7-nitroindazole increased binding of 3H-muscimol, 3H-pirenzepine and 3H-kainate, whereas the less isoform-specific, general NOS-inhibitor L-nitroarginine increased binding of 3H-muscimol and 3H-AMPA in most cortical areas, leaving 3H-kainate binding almost unchanged. The water soluble L-nitroarginine-methylester caused similar effects to those of L-nitroarginine which changed over a period of chronic treatment. The inhibitory GABAA-receptors were increased after NOS-inhibition in most cortical areas, whereas binding of 3H-Oxotremorine-M (acetylcholine receptors), 3H-MK-801 (NMDA-receptors) and 3H-AMPA (AMPA receptors) was affected differently among the cortical areas. Strongest alterations of ligand-binding capacity after administration of NOS-inhibitors were seen in cortical areas known to contain the highest packing densities of NOS-I-positive interneurons such as the piriform and entorhinal cortices, indicating that, in normal animals, neurotransmission and probably cognitive information processing would be affected by the pharmacological modulation of nitric oxide production.

Animals↗

Patterned distribution of immunoreactive astroglial processes in the striate (V1) cortex of New World monkeys.

The possibility of a modular organization of non-neuronal elements was analyzed in the opercular region of the striate neocortex in adult New World monkeys. For this purpose, and in order to follow possible correlations in the general organization of neuronal and astroglial elements, immunocytochemical procedures for Glial Fibrillary Acid Protein (GFAP) and Microtubule Associated Protein 2 (MAP-2), in addition to cytochrome oxidase (COX) histochemistry, were applied to tangential and coronal sections and analyzed by using computer-assisted procedures. Astroglial interlaminar processes stemming from superficial laminae did not traverse lamina IVA, and thus did not appear in deeper layers. Clearly definable interlaminar processes were predominantly concentrated in laminae II-III. A honeycomb- like lattice was observed in tangential sections, with a "cell" size distribution similar to the MAP-2-IR lattice, suggesting an intimate association with the pyramidal columns. Additionally, analysis of similar sections disclosed the periodic appearance of large patches with high density of interlaminar processes, indicating a nonhomogeneous distribution of GFAP-IR processes in the striate cortex. COX "blobs" appeared frequently to coincide with areas expressing high density of GFAP-IR elements. These findings add a new perspective to current concepts of astroglial organization in the striate cortex of primates and reveal the existence of a non-neuronal modular organization in the primate striate cerebral cortex, and suggest that possible correlations between relative distributions of neuronal and astroglial elements should be further analyzed in cortical areas with a clear modular organization such as the striate cortex.

Animals↗

Receptor autoradiographic mapping of the mesial motor and premotor cortex of the macaque monkey.

This study analyzes regional and laminar distribution patterns of neurotransmitter binding sites in the motor areas of the macaque mesial frontal cortex. Differences in distribution patterns are compared with the cytoarchitectonic parcellation. Binding sites were analyzed with quantitative in vitro receptor autoradiography in unfixed brains of five macaque monkeys. Alpha-amino-3-hydroxy-5-methyl-4-isoxalone propionic acid (AMPA), kainate, and N-methyl-D-aspartate (NMDA) binding sites were labeled with [3H]AMPA, [3H]kainate, and [3H]MK-801, respectively, muscarinic binding sites with [3H]pirenzepine or [3H]oxotremorine-M, noradrenergic binding sites with [3H]prazosin or [3H]UK-14304, gamma-aminobutyric acid (GABA)A binding sites with [3H]muscimol, and serotoninergic binding sites with [3H]ketanserine. Adjacent sections were stained with a modified Nissl method for cytoarchitectonic analysis. In the motor areas F1, F3, and F6, [3H]AMPA, [3H]pirenzepine, and [3H]oxotremorine-M binding was maximal in layers II, III, and V, and [3H]kainate binding was maximal in layers V and VI. Clear-cut changes in laminar distribution patterns of [3H]AMPA, [3H]kainate, and [3H]oxotremorine-M binding sites very closely matched corresponding cytoarchitectonic borders. Mean areal binding densities of all ligands to F1, F3, and F6 were plotted as polar plots for each area. A polygon was obtained for each area ("neurochemical fingerprint") when all the density values belonging to one area were connected with each other. The "neurochemical fingerprints" of F1, F3, and F6 were virtually identical in shape but increased in size from F1 to F6. This result reflects the functional similarity of these motor-related areas and possibly correlates with their differential involvement in motor control. Areas F1, F3, and F6 can thus be grouped into one "neurochemical family" of areas.

Animals↗

Limbic frontal cortex in hominoids: a comparative study of area 13.

The limbic frontal cortex forms part of the neural substrate responsible for emotional reactions to social stimuli. Area 13 is one of the cortical areas long known to be part of the posterior orbitofrontal cortex in several monkey species, such as the macaque. Its presence nevertheless in the human brain has been unclear, and the cortex of the frontal lobe of the great and lesser apes remains largely unknown. In this study area 13 was identified in human, chimpanzee, bonobo, gorilla, orangutan, and gibbon brains, and cortical maps were generated on the basis of its cytoarchitecture. Imaging techniques were used to characterize and quantify the microstructural organization of the area, and stereological tools were applied for estimates of the volume of area 13 in all species. Area 13 is conservative in its structure, and features such as size of cortical layers, density of neurons, and space available for connections are similar across hominoids with only subtle differences present. In contrast to the homogeneity found in its organization, variation is present in the relative size of this cortical area (as a percentage of total brain volume). The human and the bonobo include a complex orbitofrontal cortex and a relatively smaller area 13. On the contrary the orangutan stands out by having a shorter orbitofrontal region and a more expanded area 13. Differences in the organization and size of individual cortical areas involved in emotional reactions and social behavior can be related to behavioral specializations of each hominoid and to the evolution of emotions in hominids.

Anatomy, Comparative↗

Structural alterations and changes in cytoskeletal proteins and proteoglycans after focal cortical ischemia.

In order to study structural alterations which occur after a defined unilateral cortical infarct, the hindlimb region of the rat cortex was photochemically lesioned. The infarcts caused edema restricted to the perilesional cortex which affected allocortical and isocortical areas differently. Postlesional changes in cytoskeletal marker proteins such as microtubule-associated protein 2, non-phosphorylated (SMI32) and phosphorylated (SMI35, SMI31 and 200,000 mol. wt) neurofilaments and 146,000 mol. wt glycoprotein Py as well as changes in proteoglycans visualized with Wisteria floribunda lectin binding (WFA) were studied at various time points and related to glial scar formation. The results obtained by the combination of these markers revealed six distinct regions in which transient, epitope-specific changes occurred: the core, demarcation zone, rim, perilesional cortex, ipsilateral thalamus and contralateral homotopic cortical area. Within the core immunoreactivity for microtubule-associated protein 2 and SMI32 decreased and the cellular components showed structural disintegration 4 h post lesion, but partial recovery of somatodendritic staining was seen after 24 h. Microtubule-associated protein 2 and SMI32 persisted up to days 7 and 5 respectively in the core, whereas the number of glial fibrillary acidic protein- and WFA-positive cells decreased between days 7 and 14. The demarcation zone showed a dramatic loss of immunoreactivity for all epitopes 4 h post lesion which was not followed by a phase of recovery. In the inner region of the demarcation zone there was an invasion and accumulation of non-neuronal WFA-positive cells which formed a tight capsule around the core. Neuronal immunoreactivities for microtubule-associated protein 2, SMI31 and Py as well as astrocytic glial fibrillary acidic protein increased strongly within an approximately 0.4-1.0 mm-wide rim region directly bordering the demarcation zone. Py immunoreactivity increased significantly in the perilesional cortex, whereas glial fibrillary acidic protein-positive astrocytes became transiently more numerous in the entire lesioned hemisphere including strongly enhanced immunoreactivity in the thalamus by days 5-7 post lesion. Glial fibrillary acidic protein immunoreactivity increased in the corpus callosum and the homotopic cortical area of the unlesioned hemisphere by days 5-7. In this homotopic area additional changes in SMI31 immunoreactivity occurred. Our results showed that a cortical infarct is not only a locally restricted lesion, but leads to a variety of cytoskeletal and other structural changes in widely-distributed functionally-related areas of the brain.

Animals↗

Modular distribution of vasoactive intestinal polypeptide in the rat barrel cortex: changes induced by neonatal removal of vibrissae.

The distribution of vasoactive intestinal polypeptide-immunoreactive neuronal structures in the barrel cortex (posteromedial barrel subfield) of adult rats was analysed after unilateral removal of the vibrissal follicles of row C in neonatal rats. The hypothesis was tested whether the distribution of vasoactive intestinal polypeptide-immunoreactive structures depends on the normal anatomical organization of the specific sensory input. After three months survival the distribution of the vasoactive intestinal polypeptide-immunoreactive structures was morphometrically evaluated. This approach revealed alterations in the contralateral posteromedial barrel subfield, where the disappearance of barrel row C and a substantial increase in size mainly of barrel row D, but also of other rows could be detected. Increase in row D included both barrels and the interspace (septal segments between barrels in one row). As vasoactive intestinal polypeptide immunoreactivity of the barrel field was found previously to be localized in synaptic boutons involved in symmetric synapses, our present findings suggest that (i) the interspace is enriched in inhibitory vasoactive intestinal polypeptide-immunoreactive synapses as opposed to the excitatory thalamocortical input reaching the barrel hollow, (ii) the spatial distribution of the vasoactive intestinal polypeptide system in the barrel cortex is closely associated with the neuronal organization of the sensory input and reacts with a considerable plasticity to lesion-induced changes of the input, and (iii) the compensatory barrel hypertrophy in a row neighbouring the deafferented row involves an increasing number of vasoactive intestinal polypeptide-immunoreactive synapses per barrel.

Afferent Pathways↗

Long-term changes of ionotropic glutamate and GABA receptors after unilateral permanent focal cerebral ischemia in the mouse brain.

Long-term hyperexcitability was found after unilateral, permanent middle cerebral artery occlusion in exofocal neocortical areas of the adult mouse [Mittmann et al. (1998) Neuroscience 85, 15-27]. The aim of the present study was to test the hypothesis in an identical paradigm of ischemia. whether alterations in the densities of both excitatory and inhibitory amino acid receptors may underlie these pathophysiological changes. Alterations in densities of [3H]dizocilpine, [3H]D,L-amino-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid, [3H]kainate and [3H]muscimol binding sites were demonstrated with quantitative in vitro receptor autoradiography. All binding sites were severely reduced in the core of the ischemic lesion. A completely different reaction was found in the exofocal, histologically inconspicuous parts of the somatosensory cortex and the more remote neocortical areas of both hemispheres. The [3H]muscimol binding sites were significantly reduced four weeks after ischemia in the motor cortex, hindlimb representation area and exofocal parts of the primary and secondary somatosensory cortices of both hemispheres. The focus of the reduction in [3H]muscimol binding sites was found in lower layer V and upper layer VI. Contrastingly, the densities of [3H]dizocilpine binding sites were found to be increased in these areas, whereas those of [3H]D,L-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid and [3H]kainate binding sites did not show significant changes. The [3H]dizocilpine binding site density increased predominantly in layers III and IV. All binding sites were also reduced in the retrogradely reacting, gliotic part of the ipsilateral ventroposterior thalamic nucleus, whereas the [3H]D,L-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid binding sites were increased in the surround of the ipsilateral nucleus and no changes in binding sites were seen in the whole contralateral nucleus. We conclude that permanent local ischemia leads to a long-term and widespread impairment of the normal balance between binding sites of excitatory and inhibitory neurotransmitter receptors in neocortical areas far away from the focus of the post-ischemic tissue damage. The imbalance comprises an up-regulation of the [3H]dizocilpine binding sites in the ion channels of N-methyl-D-aspartate receptors and a down-regulation of [3H]muscimol binding sites of the GABA(A) receptors in the ipsi- and contralateral neocortex. These changes at the receptor level explain the previously observed hyperexcitability with the appearance of epileptiform field potentials and the long duration of excitatory postsynaptic potentials four weeks after ischemia.

Animals↗

Characterization of neuronal migration disorders in neocortical structures: quantitative receptor autoradiography of ionotropic glutamate, GABA(A) and GABA(B) receptors.

Epileptiform activity was previously described [Luhmann et al. (1998) Eur. J. Neurosci., 10, 3085-3094] in the neocortex of the adult rat following freeze lesioning of the newborn neocortex. After a survival time of 3 months, a small area of dysplastic cortex surrounded by histologically normal (exofocal) neocortex was observed. The dysplastic cortex is characterized by the formation of a small sulcus and a three- to four-layered architecture. Two questions are addressed here: (i) is the hyperexcitability associated with changes in binding to major excitatory and inhibitory transmitter receptors in the dysplastic cortex?; and (ii) do such changes also occur in the exofocal cortex? Alterations in binding to glutamatergic N-methyl-D-aspartate (NMDA), (+/-)-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA), kainate and GABA(A) and GABA(B) (gamma-aminobutyric acid) receptors are demonstrated with quantitative in vitro receptor autoradiography by using the ligands [3H]MK-801, [3H]AMPA, [3H]kainate, [3H]muscimol and [3H]baclofen, respectively. In the dysplastic cortex, the binding to NMDA, AMPA and kainate receptors is significantly increased, whereas the binding to GABA(A) and GABA(B) receptors is reduced. Exofocal areas of the lesioned hemisphere show an imbalance between excitatory and inhibitory receptor binding with an up-regulation of the binding to AMPA and kainate, and a down-regulation to GABA(A) receptors. The binding to GABA(B) and NMDA receptors is not significantly changed in the exofocal areas. The imbalance between excitatory and inhibitory receptors may cause the hyperexcitability, as previously found in the identical experimental model, and may also induce epileptiform activity in the human cortex with migration disorders.

Animals↗

Tissierella creatinophila sp. nov., a gram-positive, anaerobic, non-spore-forming, creatinine-fermenting organism.

A strictly anaerobic, Gram-positive, non-spore-forming bacterium was isolated from sewage sludge which grew on creatinine as sole source of carbon and energy. This new isolate, designated strain KRE 4T, totally degraded creatinine via creatine, sarcosine and glycine to the products acetate, monomethylamine, ammonia and carbon dioxide. Growth on creatinine or creatine was selenium-dependent and stimulated by formate, indicating the involvement of a creatine reductase, sarcosine reductase and/or glycine reductase. This was substantiated by the fact that creatine, sarcosine and glycine were reduced by cell-free extracts. Growth on creatinine or creatine was also possible in the absence of formate, but with an increase in doubling time. The new bacterium occurred as rod-shaped cells, which exhibited an angular form (2-6 microns long and 0.7-1.1 microns wide) and showed motility by means of peritrichous flagella. The G+C content of the DNA was 30 mol %. Comparative 16S rRNA sequence analysis demonstrated that strain KRE 4T represents a new subline within the genus Tissierella. Due to its very restricted substrate spectrum and the inability of whole cells to utilize sarcosine and glycine as intermediates of creatine breakdown, this organism can be readily separated from currently described species of Tissierella. Therefore, based on the phenotypic and phylogenetic distinctiveness of the new isolate, it si proposed that the bacterium be classified as a new species of the genus Tissierella, Tissierella creatinophila sp. nov. The type strain is KRE 4 (= DSM 6911T).

Base Sequence↗

Transient increase of manganese-superoxide dismutase in remote brain areas after focal photothrombotic cortical lesion.

BACKGROUND AND PURPOSE: Free radicals including superoxide are responsible for postlesional cytotoxicity. In contrast to the constitutive CuZn-superoxide dismutases (SODs), manganese-superoxide dismutase (Mn-SOD) is inducible and has the potential to protect neurons by its superoxide dismutating activity. Therefore, we studied the presence and the regional changes in Mn-SOD within the brain after focal cortical ischemia. METHODS: Focal cortical photothrombotic lesions were produced in the hindlimb region of rat brains. Animals were anesthetized and transcardially perfused with Zamboni's fixative. Mn-SOD was immunohistochemically localized using an antiserum against rat-Mn-SOD. Changes in Mn-SOD immunoreactivity were quantified by image analysis. RESULTS: Focal photothrombosis caused a perilesional increase in Mn-SOD after 24 hours, followed by a further significant increase at 48 hours in perilesional cortex, ipsilateral corpus callosum, hippocampus, and thalamus, as well as in a homotopic cortical area within the nonlesioned hemisphere. At day 2, Mn-SOD was present in neurons and astrocytes. Up to day 7, Mn-SOD increased in the entire ipsilateral and contralateral cortex but remained higher elevated in the ipsilateral hippocampus and thalamus. Thereafter, Mn-SOD decreased globally but remained elevated in some cortical neurons up to day 60. CONCLUSIONS: The early transient increase of Mn-SOD in distinct brain regions, which are functionally connected via afferents and efferents, suggests that these regions are affected by the injury. It suggests that Mn-SOD protects the cells in these regions from superoxide-induced damage and therefore may limit the retrograde and anterograde spread of neurotoxicity.

Animals↗

The size of the middle temporal area in primates.

The increase in the size of the lateral geniculate body and the primary visual cortex from prosimians to apes and man reflects at an anatomical level the importance of the visual system in primates. In the prestriate cortex visual modalities are processed separately in specialized pathways and areas. This arrangement facilitates the allometric analysis of cortical areas subserving defined visual modalities. Its heavy myelination makes the middle temporal area, a visual cortical field specialized for the detection of moving stimuli, an easily detectable and reliably delineable area in histological sections. The size and position of the middle temporal area can therefore be compared between species, in order to collect quantitative data about the development of a defined visual submodality during primate evolution. The volume of the middle temporal area was measured in 27 primate species. Allometric comparisons show that the middle temporal area is larger in simians than in most prosimians. In Callitrichidae, both the middle temporal area and the striate cortex are well developed. In cebids and cercopithecids, however, the sizes of the middle temporal area and primary visual cortex show divergent trends. Whereas the striate cortex is still enlarging, the size of the middle temporal area is reduced as compared to callitrichids. Previous studies have revealed a close correlation between area striata and neocortex sizes, as well as area striata and lateral geniculate sizes. Such a close correlation does not exist for the middle temporal area versus neocortex or area striata. Therefore, the size of a visual structure serving a special submodality (e.g., the middle temporal area for the detection of moving stimuli) may develop in a species relatively independently from the lateral geniculate and primary visual cortex sizes.

Animals↗

The distribution of nitric oxide synthase-I and NADPH-diaphorase containing neurons in the cerebral cortex of different strains of mice and its association with learning and memory.

We investigated the distribution of nitric oxide synthase-I (NOS-I) containing neurons within the neocortex of inbred mice belonging to the Balb/c, NMRI and DBA/2 strains which differ in learning and memory performance. The NOS-I positive neurons were detected immunohistochemically with antibodies against NOS-I and enzyme histochemically using their NADPH-diaphorase (NADPH-d) activity. The qualitative and quantitative evaluation of cortical NADPH-d and NOS-I containing neurons revealed that more than 95% of these cells contained both enzymes. Therefore, we combined the NADPH-d with the WFA-staining to evaluate and parcellate at one section. The specific differences in learning and memory tasks of the three mouse strains have been tested in previous studies. Our investigation test the hypothesis that differences in various aspects of eight-arm radial maze learning are associated with differences in the density of NOS-I positive neurons in cytoarchitectonically and functionally identified cortical areas. We found an increased density of NADPH-d neurons within the whole neocortex in the DBA/2 strain, which reached a lower learning score than the Balb/c and NMRI strains. Significantly higher densities of NADPH-d neurons appeared in the areas of the gustatory cortex, the piriform cortex, the entorhinal cortex and in area 1 of the temporal cortex in DBA/2 mice. A negative correlation exists between the learning scores and the number of NADPH-d positive neurons. If NOS-I activity influences spatial learning as determined in the eight-arm radial maze, the areas with strongly elevated NADPH-d positive neurons may demarcate task-related cortical areas affected in mice with a reduced learning capacity.

Animals↗

Copper-zinc superoxide dismutase and isolectin B4 binding are markers for associative and transhemispheric diaschisis induced by focal ischemia in rat cortex.

Copper/zinc-superoxide dismutase (Cu/Zn-SOD) belongs to a class of enzymes, identified as essential and highly effective endogenous scavengers of cytotoxic oxygen radicals. These radicals contribute to postlesional neurotoxicity. In order to determine the superoxide-scavenging potential of regions affected by unilateral cortical photothrombosis, we studied the changes in the distribution of Cu/Zn-SOD and the appearance of activated microglia by immunohistochemistry and isolectin B4 binding. Four hours postlesion, Cu/Zn-SOD increased significantly within a homotopic area of the contralateral hemisphere and in ipsilateral thalamic nuclei, whereas isolectin B4-positive microglia were upregulated at days 5 and 7 postlesion within the same regions. The contralateral increase in the amount of the superoxide-scavenging Cu/Zn-SOD indicates that this enzyme is induced by a retrograde reaction carried through callosal connections.

Animals↗

The somatosensory cortex of human: cytoarchitecture and regional distributions of receptor-binding sites.

The aim of this study is to characterize the regional and laminar distribution patterns of various neurotransmitter binding sites in areas 3a, 3b, 1, and 2 of the human primary somatosensory cortex, and to compare these receptor-based "maps" with the cytoarchitectonic parcelation. Cryostat sections from a dorsomedial region of the postcentral gyrus close to the interhemispheric fissure and from a ventrolateral region close to the Sylvian fissure were examined. Neurotransmitter-binding sites were analyzed with quantitative in vitro receptor autoradiography. Different muscarinic-binding sites were labeled with [3H]pirenzepine and [3H]oxotremorine-M, noradrenergic-binding sites with [3H]prazosin, different serotoninergic-binding sites with [3H]5-hydroxytryptamine and [3H]ketanserine, glutamate-binding sites with l-[3H]glutamate, and GABA-binding sites with [3H]muscimol. Adjacent sections were stained with a modified Nissl method for cytoarchitectonic analysis. The binding sites either were preferentially localized in the superficial layers ([3H]5-hydroxytryptamine, [3H]prazosin, l-[3H]glutamate, [3H]muscimol, and [3H]pirenzepine) or were more homogeneously distributed with highest densities in layers III-V ([3H]oxotremorine-M and [3H]ketanserine). Changes in the distribution patterns of [3H]oxotremorine-M- and [3H]ketanserine-binding sites precisely matched the borders between areas 4/3a, 3b/1, and 1/2, as defined cytoarchitectonically. In addition, the autoradiographs showed that area 1 possibly consists of two subregions which cannot be distinguished cytoarchitectonically. The results demonstrate that the regional and laminar distribution patterns of some, but not all, transmitter-binding sites are precisely correlated with the cytoarchitectonic parcelation of the human primary somatosensory cortex. In addition, binding sites may reveal new borders not detectable in Nissl-stained sections. Finally, the human primary somatosensory cortex differs clearly from the primary motor cortex due to higher densities of l-[3H]glutamate-, [3H]muscimol-, [3H]pirenzepine-, [3H]oxotremorine-M-, and [3H]ketanserine-binding sites.

Aged↗

Postnatal development of interhemispheric asymmetry in the cytoarchitecture of human area 4.

The postnatal development of interhemispheric asymmetry was analyzed in the primary motor cortex (area 4) of 20 human brains with quantitative cytoarchitectonic techniques. The volume fraction of cortical tissue occupied by cell bodies (grey level index) was determined by automated image analysis. In children as well as in adults, the volume fraction of cell bodies averaged over all cortical layers was greater on the right than on the left. Thus, the space between cell bodies, i.e. the volume fraction of neuropil containing axons, dendrites and synapses, was greater in the left than in the right primary motor cortex. At the level of single layers, however, interhemispheric asymmetry of the neuropil volume fraction differed between age groups. The supragranular layers were significantly less asymmetrical in children than in adults, whereas the infragranular layers showed a similar degree of asymmetry in both age groups. Thus, the postnatal development of the architectonic asymmetry in the supra- and infragranular layers of area 4 follows the same sequence of maturation as found during neuronal migration, i.e. an inside-to-outside gradient. Comparing the layer-specific developmental pattern with available functional data, it was found that the structural maturation of interhemispheric asymmetry in the supragranular layers correlates with the development of hand preference.

Adult↗