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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Cellular and molecular life sciences 42 (1986), S. 37-39 
    ISSN: 1420-9071
    Keywords: Serum ; intrathecal injection ; CNS ; dissociated myelin ; demyelination ; multiple sclerosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Normal human or rat serum administered by intraventricular injection induced demonstrable changes in the rat CNS myelin as seen from an increased recovery of dissociated myelin (DM), i.e. a myelin-related low density membrane fragments, from the tissue homogenates. The yield of DM reached a maximum on the third postinjection day and returned to the control level by day 5. In spite of the increased recovery of DM, no physico-chemical alternations in myelin isolates and no histological abnormalities in the tissue could be detected. The production of DM seems to be a sensitive index of serum-induced alteration of the myelin sheath.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0533
    Keywords: Blood-brain barrier ; Lymphocytic choriomeningitis ; Mice
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The ultrastructure and the blood-brain-barrier (BBB) permeability were studied in mice suffering from lymphocytic choriomeningitis (LCM). Brains and meninges from mice suffering from LCM virus-induced lymphocytic choriomeningitis were studied by investigating the BBB function and by electron and light microscopy. The cellular exudate in the leptomeninges was located in the subarachnoid space, in arachnoidea and pia, and it was dominated by proliferated pial cells and mononuclear cells, most of which were lymphocytes, while there were only a few neutrophil granulocytes. Many intravascular lymphocytes were seen adhering to as well as penetrating the vessel walls. Many of these lymphocytes were morphologically compatible with T cells. Lymphocytes and larger mononuclear cells were also accumulated in the choroid plexus, and lymphocytes were present in the ventricular system with a tendency to adhere to ependymal epithelial cells. Inspection of the ultrathin sections incubated for horseradish peroxidase (HRP)-activity revealed that the overwhelming part of the peroxidase activity was localized in the extracellular space of the meningeal vessel walls and especially in the abundant intercellular fluid which, like the inflammatory cells, was found in the subarachnoid space in arachnoidea and in pia. In the neuropil, only very small quantities of reaction product were seen intercellularly in the most superficial layers of the cortex. The tight junctions were always intact, but the possibility of a non-demonstrable opening is discussed. Evaluation of the BBB permeability for 2-amino[1-14C]isobutyric acid (AIB) was made by quantitative autoradiography, and it was demonstrated convincingly that AIB concentrations in the subpial and perichoroidal tissues were markedly increased in diseased animals as compared to the controls. Our results seem to contradict previous theories on the cause of death resulting from the LCM disease. The findings presented here do not speak in favor of a pronounced brain edema, just as results obtained by us and others do not speak for the possibility of the death being caused by convulsive seizures with subsequent brain anoxia. However, our observations are compatible with the hypothesis that cytotoxic T cells may interact in vivo with virus-infected targets, which are essential for the regulation of the composition of the cerebrospinal fluid. On the other hand, the dysfunction of the BBB demonstrated adds a new element to the pathologic mechanism in a model for the study of virus-induced meningitis.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0533
    Keywords: Kainic acid ; non-N-methyl-d-aspartate antagonists ; α-Amino-3-carboxy-methoxy-5-methyl-4-isoxazolepropionic acid (AMOA) ; α-Amino-2-(3-hydroxy-5-methyl-4-isoxazolyl)methyl-5-methyl-3-oxo-4-isoxazoline-4-propionic acid (AMNH) ; Striatum
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The possible neuroprotective effects of two new non-N-methyl-d-aspartate receptor antagonists were determined by quantitative light microscopy after intracerebral administration of kainic acid (KA) in two rat brain regions. KA alone or KA in combination with the antagonists α-amino-3-carboxy-methoxy-5-methyl-4-isoxazolepropionic acid (AMOA) and α-amino-2-(3-hydroxy-5-methyl-4-isoxazolyl)methyl-5-methyl-3-oxo-4-isoxazoline-4-propionic acid (AMNH) were stereotaxically injected into the striatum or into the CA3 region of hippocampus. Seven days later neuropathological examination including cell counts was performed on paraffin sections from the two brain regions. In the striatum, AMOA almost completely attenuated KA-induced cell damage, whereas AMNH showed no protective effect. In the hippocampal CA3 region none of the test compounds possessed neuroprotective properties against KA. These results seem to be consistent with a difference in the mechanisms responsible for the neurotoxic action of KA in the hippocampus compared to the striatum.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 40 (1977), S. 117-122 
    ISSN: 1432-0533
    Keywords: Brain cortex ; Brain capillaries ; Alkaline phosphatase ; Porto-caval anastomosis ; Morphometry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Morphometric investigation by automatic image analysis of alkaline phosphatase positive brain capillaries was performed in control rats and in rats with a 30 days old porto-caval anastomosis. Rats with a porto-caval anastomosis showed an increased capillary diameter Di and as a consequence of this a decreased capillary surface-to-volume ratio Si/Vi. The free capillary distance was increased and the capillary length per unit brain volume LVi was decreased in the shunted rats compared to the controls. There was no difference in the percentage of the projected capillary area $$A_{A_i }$$ % between the two groups. It is suggested that the dilatation of the capillaries in rats with a porto-caval anastomosis is caused by the altered haemodynamic properties with a low mean blood pressure although the cardiac output is increased and that the alteration in free capillary distance and length per unit brain volume LVi is caused by dispersion by cortical edema induced by the porto-caval anastomosis.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-0533
    Keywords: Ischemia ; Brain ; Hippocampus ; Synapses ; Ultrastructure ; Morphometry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A 10-min long ischemic insult followed by up to 60-min survival results in several changes of the synaptic ultrastructure in the hippocampal CA-1 region. The alternations consist of gradual change of synaptic curvature from neutral to positive, cleavage and decrease in thickness of the postsynaptic densities and, in the case of many terminals, wrinkling of their profiles. The most striking form of damage are membrane discontinuities which begin to appear in very small numbers after 20 min of blood reflow and become much more pronounced after 60 min. The development of those modifications seems to be time-related, whereas decrease in the number of synaptic vesicles, as shown by the morphometric analysis, occurs after 10 min and does not progress any further after 20 and 60 min. This decrease is most pronounced in the immediate vicinity of the presynaptic membrane. Although the observed signs of ultrastructural alternations of synapses in the postischemic period appear to conform to the general pattern of synaptic degeneration observed under other conditions, the severity of ischemia is underlined with the rate at which those changes develop, thus pointing toward grossly disturbed metabolism of postischemic neurons. Recently, a number of theories have been advanced, discussing significance of ischemic destruction of membrane phospholipids. These theories are discussed in the context of membrane discontinuities reported in this investigation.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 74 (1987), S. 234-238 
    ISSN: 1432-0533
    Keywords: Microdialysis ; Hippocampus ; Tissue reaction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Microdialysis tubes, used for measurements of extracellular neurotransmitter concentrations, were implanted in rat dorsal hippocampus to study the adjacent tissue reaction. The brain was examined 1–60 days after the implantation. Within the first 2 days, normal neuropil and only occasional hemorrhage surrounded the microdialysis tube. Three days following the implantation astrocytes close to the dialysis tube, hypertrophied. Hypertrophic astrocyte processes invaded the spongy fiber wall. There was no increase in the number of astrocytes. Fourteen days after the fiber insertion layers of reticulin-positive fibers separated astrocytes and the remaining neuropil from the fiber wall. Late tissue changes (1 and 2 months) consisted of collagen deposits and occasional granuloma formation. These results can be used to predict the optimal time for commencing microdialysis after the fiber implantation.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 73 (1987), S. 189-194 
    ISSN: 1432-0533
    Keywords: Cerebral ischemia ; Hippocampus ; Entorhinal cortex ; CA-1 pyramidal cell protection
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The excitatory (glutamatergic) innervation seems to determine a nerve cells vulnerability to complete, transient ischemia. Interruption of the excitatory afferents to the hippocampus by removal of the entorhinal cortex prior to ischemia allows examination of this hypothesis. Groups of adult male Wistar rats were subjected to 20 min of ischemia (fourvessel occlusion) 4 days following a sham procedure, unilateral or bilateral entorhinotomy. CA-1 pyramidal cell survival following ischemia was assessed by light microscopic examination (cell counts) 4 days after ischemia. Compared to control animals unilateral entorhinotomy protected 50% of the CA-1 pyramidal neurons ipsilateral to the lesion, whereas bilateral entorhinotomy resulted in 84% protection. The pathophysiology of ischemic brain damage is discussed, and it is suggested that the protection of CA-1 pyramidal neurons after entorhinotomy is due to interruption of the input to the dentate granule cells, which forms a link in the trisynaptic pathway from the entorhinal cortex to the CA-1.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 39 (1977), S. 59-68 
    ISSN: 1432-0533
    Keywords: Porto-caval anastomosis ; Glial ; Neurone changes ; Porto-systemic encephalopathy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Nuclear size and density were determined in brain regions with different glial—neurone composition in rats up to 35 weeks after porto-caval anastomosis. In the white matter, i.e. corpus callosum, both the total cell count and the percentage of astrocytes and oligodendrocytes were unchanged. In the corpus striatum, where the glial/neurone ratio is about 1, the number of nuclei registered as astrocytes increased, and after 35 weeks astrocytes comprised 29% of glial cells (compared with 15% in controls). However, the number of oligodendrogial nuclei decreased simultaneously, leaving the total glial number unchanged. In the animals with longest experimental period there was a 15% loss of neurones. In a region with higher glial/neurone ratio, i.e. the Purkinje cell layer, the neurones showed a similar reduction, whereas the number of Bergmann astrocyte nuclei increased less than striatal astrocytes. A small group of animals with pronounced signs of encephalopathy had a higher loss of neurones and, furthermore, the glial number in corpus striatum and callosum was reduced, due to loss of oligodendrocytes. Despite the use of perfusion fixation, the size of astrocyte nuclei increased, this was reversible, as only slight changes were seen after 35 weeks. A possible explanation of the increase in astrocyte nuclear count and decrease in oligodendroglial count could be that nuclei normally considered to the oligodendroglial are transformed into nuclei with morphological characteristics of astrocytes.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 61 (1983), S. 135-140 
    ISSN: 1432-0533
    Keywords: Cerebral ischemia ; CA-1 interneurons ; Hippocampus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The aim of this morphological study was to determine the vulnerability of hippocampal interneurons to ischemia in the adult rat. Two types of interneurons situated in the CA-1 stratum oriens were investigated, the larger basket cells close to stratum pyramidale and the smaller basket cells close to the alveus. Male Wistar rats were subjected to 20 min of transient cerebral ischemia by means of 4-vessel occlusion and perfusion fixed 1, 2, 4, or 21 days later. In both Golgi-impregnated and in routinely stained sections the pyramidal cells and interneurons in the hippocampal CA-1 region were examined and counted. The study clearly demonstrated the selective vulnerability of the CA-1 pyramidal cells, as no ischemic cell damage to or loss of interneurons was found.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 71 (1986), S. 46-54 
    ISSN: 1432-0533
    Keywords: Seizures ; Kainic acid ; Glucose ; Hippocampus ; Interneurons
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Systemic administration of kainic acid (KA), 11 mg/kg body weight, to hyperglycemic rats induced lethal seizures in all animals, while 40% of normoglycemic rats survived the KA treatment and all hypoglycemic rats survived. An inverse correlation (P〈0.01) between the plasma glucose level and survival during KA-induced seizures was demonstrated (Chi-square-test). Histopathological observations on the surviving rats clearly divided them into a group with severe hippocampal CA-1 damage and a group with mild hippocampal CA-1 damage. Hippocampal pyramidal cells and CA-1 interneurons were counted 3 weeks after the insult. The pyramidal cell loss in the CA-1 region was significant within mildly, as well as severely, affected rats with normo- and with hypoglycemia. CA-1 interneurons and CA-4 interneurons were only lost in the severely affected group. Hypoglycemia seemed to protect those CA-1 interneurons situated close to the alveus and within the stratum radiatum in these animals. The increased mortality in the hyperglycemic rats could be due to increased brain lactate accumulation, but extracerebral damage of hyperglycemia in association with KA is also a possibility. The study indicated a correlation between loss of interneurons and pronounced CA-1 pyramidal cell death and furthermore that hypoglycemia possibly protected some interneurons against KA.
    Type of Medium: Electronic Resource
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