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  • 1980-1984  (4)
  • Brain edema  (3)
  • Axonal transport  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Pathogenesis of brain lesions caused by experimental epilepsy (1981)
    Springer
    Acta neuropathologica 54 (1981), S. 219-231 
    Details
    ISSN: 1432-0533
    Keywords: Status epilepticus ; Nerve cell injury ; Brain edema ; Rat cerebral cortex
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Status epilepticus was induced in rats by the GABA receptor blocking agent, bicuculline, during artificial ventilation and with closely monitored physiologic parameters. After 1 or 2 h of status epilepticus the brains were fixed by perfusion with glutaraldehyde and processed for light and electron microscopy. In the cerebral cortex two different types of changes were present, i.e., nerve cell injuries and status spongiosus. Type 1 injured neurons, mainly in the areas of most marked sponginess (layer 3), displayed progressive condensation of both karyo-and cytoplasm. In the most advanced stages the nucleus could no longer be distinguished from the cytoplasm in the light microscope, and vacuoles of apparent Golgi cisterna origin appeared in the darkly stained cytoplasm. This type of injured neurons comprised 41 and 56% of the cortical neurons after 1 or 2 h of status epilepticus, respectively. Seven to 9% of the neurons showed another type of injury (type 2). They were mainly located in the deeper cortical layers, and showed slit-formed cytoplasmic vacuoles chiefly due to swelling of the endoplasmic reticulum including the nuclear envelope. Marked sponginess of the cortex developed principally in layer 3 and it spread into deeper layers with longer duration of status epilepticus, but the outermost layers retained a compact structure. As judged by electron microscopy, the sponginess resulted mainly from swelling of astrocytes and their processes causing both perivascular and perineuronal vacuolation. The structural changes observed are considered to be caused by astrocytic and to a lesser extent intraneuronal edema related to the seizure activity. Although the exact pathogenetic mechanisms are not known, our findings indicate that hypoxia-ischemia is not a major determinant of the tissue damage observed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00687745
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Pathogenesis of brain lesions caused by experimental epilepsy (1983)
    Springer
    Acta neuropathologica 59 (1983), S. 11-24 
    Details
    ISSN: 1432-0533
    Keywords: Status epilepticus ; Nerve cell injury ; Brain edema ; Rat hippocampal formation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Status epilepticus with a duration of 1 or 2 h was induced in rats by i. v. injection of the GABA receptor blocking agent, bicuculline. Immediately there-after, or following a 2 h recovery period, the brains were fixed by vascular perfusion and processed for light and electron microscopy to characterize the type and distribution of morphological changes in the hippocampal formation. In a previous study (Söderfeldt et al. 1981) astrocytic edema and wide-spread neuronal changes of two different kinds occurred in the fronto-parietal cortex of the same animals. Type 1 injured neurons were characterized by condensation of karyoplasm and cytoplasm (type 1a), which in some neurons became so intense that the nucleus could no longer be clearly discerned (type 1b). The type 2 injured neurons had slitformed cytoplasmic vacuoles chiefly caused by dilatation of the rough endoplasmic reticulum. In the hippocampus the most conspicuous alteration was astrocytic edema which was most marked around the perikarya of pyramidal neurons in CA1-CA4 and subiculum. In the dentate gyrus the edema was less pronounced and, when present, affected particularly the hilar zone of the stratum granulosum. The nerve cell changes were less pronounced than in the cerebral cortex. The vast majority of the hippocampal pyramidal neurons in CA1-CA4 showed minor configurational and tinctorial abnormalities (incipient type 1a change). Severe nerve cell alterations (type 1b) were present but very rarely affected the pyramidal neurons of CA1-CA4 and subiculum, whereas in the dentate gyrus pyramidal basket neurons of stratum granulosum and pyramidal nerve cells in stratum polymorhe showed the severe type 1b changes. As compared with the frontoparietal cortex (Söderfeldt et al. 1981) the type 2 changes were extremely rare. In the early recovery period after 1 h of status epilepticus the astrocytic edema and the incipient type 1a changes had almost entirely disappeared, whereas a few condensed and dark-staining type 1b injured neurons remained. Thus, in this model of status epilepticus the most marked response in the hippocampal formation is astrocytic edema in the layers where pyramidal perikarya are located. Incipient, mild nerve cell changes which appear to be reversible were frequent and widespread in the entire hippocampal formation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00690312
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Uptake of macromolecules into neurons from a focal vasogenic cerebral edema and subsequent axonal spread to other brain regions (1982)
    Springer
    Acta neuropathologica 57 (1982), S. 233-235 
    Details
    ISSN: 1432-0533
    Keywords: Cerebral trauma ; Vasogenic brain edema ; Axonal transport ; Blood-brain barrier ; Nerve cell injury
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Intravenously (i.v.) injected horseradish peroxidase (HRP) which has leaked out of the vessels in a cryogenic cortical injury of adult mice is taken up into a large number of neurons resulting in two different forms of labeling. Diffuse neuronal labeling of, the type previously reported in many conditions with vasogenic brain edema occurred particularly within the primary lesion. The other and more frequent type, here calledgranular neuronal labeling, was present in a wide zone immediately outside the injury. Such neurons contained HRP in numerous cytoplasmic granules and had the same characteristics as normal neurons accumulating HRP after retrograde axonal transport. By using highly sensitive histochemical methods for demonstration of HRP we could also follow bundles of labeled axons out from the primary lesion. Some of them passed the corpus callosum to the fronto-parietal cortex of the contralateral hemisphere. With this report we would like to put emphasize on certain phenomena occurring in neurons which previously have not been particularly recognized in studies on vasogenic brain edema. It can be assumed that in a focal brain lesion components from the edematous fluid and other “wound substances” can be taken up into nerve cell processes and then be intracellularly transported in different directions. In this way, nerve cell populations located in other brain areas and even in the contralateral hemisphere may be influenced by components from the primary injury.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00685395
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Measurement of edema in the nervous system (1982)
    Springer
    Acta neuropathologica 57 (1982), S. 143-150 
    Details
    ISSN: 1432-0533
    Keywords: Brain edema ; Density gradient ; Percoll ; Triethyltin intoxication
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A method is presented by which density measurements can be performed on samples from cerebral cortex and white matter of normal and intoxicated animals using nontoxic ingredients as an alternative to the bromobenzene-kerosene technique described by Nelson et al. (1971). A continuous density gradient is prepared in a calibrated glass cylinder by using a new product. Percoll, which consists of colloidal silica particles coated with polyvinyl pyrrolidone. The gradient is stable and the same column can be used for repeated experiments over a long period of time. Interactions between the gradient media and the samples are evaluated and various methodological aspects concerning removal and handling of the tissue samples are presented. Experiments with acute triethyltin (TET) intoxication in the mouse and the hamster show that the Percoll technique can be used as an alternative to the bromobenzene-kerosene method in quantitative studies on cytotoxic brain edema.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00685382
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    Paper (German National Licenses)
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