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  • Articles: DFG German National Licenses  (27)
  • 1995-1999  (5)
  • 1980-1984  (22)
  • 1
    Electronic Resource
    Electronic Resource
    Increased expression of growth-associated protein 43 immunoreactivity in axons following compression trauma to rat spinal cord (1996)
    Springer
    Acta neuropathologica 92 (1996), S. 19-26 
    Details
    ISSN: 1432-0533
    Keywords: Key words Growth-associated protein 43 ; Immunohistochemistry ; Rat ; Spinal cord ; Trauma
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Growth-associated protein 43 (GAP43) is one compound used to indicate growth of axonal endings during development and regeneration, particularly of peripheral neurons. Using immunohistochemistry, we have studied the expression of GAP43 in the spinal cord of rats subjected to mild, moderate or severe compression injury and used neurofilament immunostaining to demonstrate axonal injuries. Samples removed from the compressed T8–9, the cranial T7 and the caudal T10 segments were studied at 4 h, 24 h, 4 days and 9 days after injury. Control rats showed a moderate immunostaining of neurons in dorsal root ganglia, weak staining of ventral motor neurons and, with the exception of the corticospinal tracts, a weak staining in some axons of the longitudinal tracts of the cord. Injury in the compressed region led to increased GAP43 immunoreactivity in axons of normal and expanded size. This occurred particularly 1–4 days after injury and normalized 9 days thereafter. More marked immunostaining was present in the cranial and caudal segments. The corticospinal tracts never showed such staining. The increase of GAP43 immunostaining is presumably caused by disturbed axonal transport from neurons with the capacity to synthesize and transport the GAP43 antigen. Transported material may thus be available for regeneration of axons, but this source of material may vary between different classes of axons within the cord.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050484
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  • 2
    Electronic Resource
    Electronic Resource
    Accumulation of β-amyloid precursor protein and ubiquitin in axons after spinal cord trauma in humans: immunohistochemical observations on autopsy material (1996)
    Springer
    Acta neuropathologica 92 (1996), S. 49-55 
    Details
    ISSN: 1432-0533
    Keywords: Key wordsβ-Amyloid precursor protein ; Ubiquitin ; Human ; Spinal cord ; Trauma
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We evaluated by immunohistochemistry the presence of β-amyloid precursor protein (ßAPP) and ubiquitin-like material which may accumulate in axons of the human spinal cord subjected to injury. Autopsy material was obtained from nine cases with different types of trauma: breech delivery with neonatal spinal injury, compression of the cord induced by fractures of the vertebral column, haematomas or intradural meningioma. The post-trauma period ranged from 10 days to several years. The spinal cord of six control cases without evidence of injury presented βAPP immunoreactivity in nerve cell bodies and in a few axonal profiles but not in dendrites. Seven of the nine cases with spinal cord trauma showed an accumulation of βAPP-immunoreactive material in axons of the longitudinal tracts at the site of the injury. Five cases presented similar axonal immunoreactivity in the grey matter of the cord. Ubiquitin-like immunoreactivity was present in expanded axons in cases with spinal cord injury. Cases with spinal cord trauma thus present βAPP-immunoreactive axons particularly of the longitudinal tracts in the same way as in trauma to rat spinal cord and in various brain injuries. The aggregation of βAPP-immunoreactive material indicates disturbed axonal transport of βAPP. Accumulation of ubiquitin-like immunoreactive material in expanded axons at the site of trauma may be one prerequisite for degradation of abnormal proteins by the ubiquitin-mediated proteolytic pathway.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050488
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  • 3
    Electronic Resource
    Electronic Resource
    Bicuculline-induced epileptic brain injury (1983)
    Springer
    Acta neuropathologica 62 (1983), S. 87-95 
    Details
    ISSN: 1432-0533
    Keywords: Status epilepticus ; Nerve cell injury ; Bicuculline ; Rat cerebral cortex
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary It was earlier shown that bicuculline-induced status epilepticus gives rise to profound acute changes in the rat cerebral cortex, i.e. edema and neuronal alterations. In the present study, we explored to what extent interruption of the seizure activity reverses the changes observed. To that end, status epilepticus of 1 and 2 h duration was induced by bicuculline before the seizures were arrested by i.v. injection of diazepam. The brain was then fixed by vascular perfusion either 5 min (1 h of seizures) or 2 h (1 and 2 h of seizures) of recovery and cerebral cortical tissue was studied by light (LM) and electron microscopy (EM). Already 5 min following the arrest of seizure activity most of the astrocytic edema had disappeared, and the number of injured neurons was clearly reduced. After 2 h of recovery, following 1 h of status epilepticus, the edema was virtually absent, and only few injured cells were found (only about 1% of the neuronal population). When recovery was instituted after 2 h of status epilepticus, numerous dark, triangular neurons were found. In the last group an adequate blood pressure could not be obtained. Therefore, the cellular alterations observed were probably not the result of the seizure activityper se. After 5 min of recovery, EM studies showed condensed, dark-staining injured neurons, similar to those previously observed in non-recovery animals. However, an increased incidence of swollen mitochondria was observed. After 2 h of recovery a few severely injured neurons remained which showed signs of progressive injury with fragmentation of the cell body.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00684924
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  • 4
    Electronic Resource
    Electronic Resource
    Hypoglycemic brain injury (1980)
    Springer
    Acta neuropathologica 50 (1980), S. 31-41 
    Details
    ISSN: 1432-0533
    Keywords: Hypoglycemia ; Nerve cell injury ; Biochemistry ; Light microscopy ; Rat cerebral cortex
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Profound hypoglycemia causing the disappearance of spontaneous EEG activity was induced by insulin in rats. For analysis of cerebral cortical concentrations of labile phosphates, glycolytic metabolites and amino acids, the brain was frozen in situ. For microscopic analysis of the corresponding cerebral cortical areas the brain was fixed by perfusion. Hypoglycemia with an isoelectric EEG for 30 and 60 min caused severe perturbation of the cerebral energy metabolites. After both 30 and 60 min of isoelectric EEG, two microscopically different types of nerve cell injury were seen. Type I injury was characterized by angulated, darkly stained neurons with perineuronal vacuolation, mainly affecting small neurons in cortical layer 3. Type II injured neurons, mainly larger ones in layers 5–6, were slightly swollen with vacuolation or clearing (depending on the histotechnique used) of the peripheral cytoplasm, but had no nuclear changes. Recovery was induced by glucose injection. Improvement in the cerebral energy state occurred during the 30 min recovery period even after 60 min of hypoglycemia. However, the persisting reduction in the size of adenine nucleotide and amino acid pools after 30 or 180 min recovery suggested that some cells remained damaged. In confirmation many type I injured neurons persisted during the recovery suggesting an irreversible injury. The disappearance of virtually all type II injuries indicated reversibility of these histopathological changes. The microscopic changes in hypoglycemia were different from those in anoxia-ischemia suggesting a dissimilar pathogenesis in these states despite the common final pathway of energy failure.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00688532
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  • 5
    Electronic Resource
    Electronic Resource
    Influence of systemic factors on experimental epileptic brain injury (1983)
    Springer
    Acta neuropathologica 60 (1983), S. 81-91 
    Details
    ISSN: 1432-0533
    Keywords: Brain injury ; Status epilepticus ; Hyperoxia ; Hypoxia ; Hypotension ; Vitamin E
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A previous study from the laboratory showed that status epilepticus induced by bicuculline administration to ventilated rats produced astrocytic swelling and nerve cell changes (“type 1 and 2 injury”) particularly in layers 3 and 5 of the neocortex (Söderfeldt et al. 1981). The type 1 injured neurons were characterized by condensation of cyto-and karyoplasm and the less common type 2 cells were characterized by swelling of endoplasmic reticulum including the nuclear envelope. In the present study we explored whether changes in cerebral oxygen availability altered the extent or character of the cellular alterations. Animals with 2 h of status epilepticus were made either hyperoxic (administration of 100% O2), hypoxic (arterialpO2 50 mm Hg) or hypotensive (arterial blood pressure of either 70–75 or 50 mm Hg). Furthermore, we explored whether “oxidative” damage occurred by manipulating tissue levels of α-tocopherol, a known free radical scavenger. Non-epileptic control animals exposed to comparable degrees of hypoxia or hypotension showed no or minimal structural alterations. In the epileptic animals the results were as follows.Hyperoxia did not change the quality or extent of the structural alterations previously observed in normoxic epileptic animals. Neither administration nor deficiency ofvitamin E did modify this pattern of alterations. Inhypoxia the extent of cell damage was the same or somewhat larger than in normoxic, epileptic animals. In addition, neurons often showed cytoplasmic microvacuoles due to swelling of mitochondria. The hypoxic animals also showed swelling of astrocytic nuclei with clumped chromatin. Changes similar to those observed in hypoxic animals also appeared in moderatehypotension (mean arterial blood pressure 50 mm Hg), whereas mild hypotension (70–75 mm Hg) did not change the character of the tissue injury from that seen in hyperoxic or normoxic epileptic rats. The present results demonstrate that the neuronal cell damage that can be observed when the brain is fixed by perfusion after status epilepticus of 2 h duration is not exaggerated by hyperoxia or vitamin E deficiency nor is it ameliorated by a moderate restriction in cerebral oxygen supply or by vitamin E administration. If anything, hypoxia (or moderate hypotension) appears to increase the extent of damage and it clearly alters its ultrastructural characteristics. However, although the results fail to support the notion that epileptic cell damage is “oxidative”, definite conclusions must await information on the cell damage that remains upon arrest of the epileptic activity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00685351
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  • 6
    Electronic Resource
    Electronic Resource
    Fluorescence-microscopic localization of in vivo injected ethidium bromide in the nervous system of the mouse (1984)
    Springer
    Acta neuropathologica 63 (1984), S. 78-79 
    Details
    ISSN: 1432-0533
    Keywords: Ethidium bromide ; Cytofluorescence ; Blood-brain barrier ; Blood-nerve barrier
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Ethidium bromide is a compound which can suppress DNA, RNA, and protein synthesis in mammalian cells. It is a very useful tool in experimental neuropathology for studies on myelin lesions taking place in the spinal cord after injury to oligodendroglial cells following intracisternal or intraspinal administration. By using a technique described in this short original communication we can now directly trace the distribution of the compound in various cells of the central and the peripheral nervous systems after its administration to a living experimental animal. Therefore, in the future direct correlations can be made between the cellular distribution of the compound and its cytotoxic effects.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00688474
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  • 7
    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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  • 8
    Electronic Resource
    Electronic Resource
    Cytofluorescence localization of adriamycin in the nervous system (1983)
    Springer
    Acta neuropathologica 60 (1983), S. 125-131 
    Details
    ISSN: 1432-0533
    Keywords: Adriamycin (Doxorubicin) ; Blood-nerve barrier ; Perineurium
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Adriamycin (Doxorubicin) is a powerful anthracyclic compound, which is widely used in the treatment of maligant disease. In the rat a single systemic injection of the drug can induce pronounced lesions in peripheral ganglia, whereas in other parts of the peripheral nervous system (PNS) no changes have been reported. Since adriamycin can be directly traced in tissue sections by fluorescence microscopy it is very well suited for experimental studies on the relation between cytotoxic effects and distribution of the drug following various modes of administration. We have previously shown that after an intravenous (i.v.) injection there is an absence of adriamycin-induced nuclear fluorescence in the endoneurium of mouse sciatic nerve (Bigotte et al. 1982b). This could either be due to barrier effects in endoneurial vessels and the perineurium or to a lacking capacity of the endoneurial cell population to take up and retain adriamycin. In the present study the blood-nerve and the perifascicular diffusion barriers were therefore bypassed by endoneurial microinjections of adriamycin. After this mode of administration, Schwann cells, endoneurial mast cells, endothelial cells, and pericytes became labeled. Experimental damage of these barriers induced by ligation of the nerve also resulted in a diffusion of the drug into the endoneurial area and labeling of the same cells. The absence of nuclear binding in the endoneurium of mouse sciatic nerves after i.v. injection of adriamycin is therefore most probably due to a low or absent passage of the drug from the blood into the endoneurium, i.e., a combined barrier action of endoneurial vessels and the perineurium. Other experiments with epineurial application of the drug showed that thin intramuscular (i.m.) nerve branches differ from the sciatic nerve fascicles in allowing small amounts of adriamycin to enter the endoneurium. The present observations are of interest since it can be assumed that patients receiving adriamycin as a cytostatic drug may suffer nerve lesions whenever defects of nerve barriers are present.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00685356
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  • 9
    Electronic Resource
    Electronic Resource
    The distribution of hypoglycemic brain damage (1984)
    Springer
    Acta neuropathologica 64 (1984), S. 177-191 
    Details
    ISSN: 1432-0533
    Keywords: Hypoglycemia ; Cerebral damage ; Cerebrospinal fluid ; Interstitial fluid ; Neuronal necrosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Rats were exposed to insulin-induced hypoglycemia resulting in periods of cerebral isoelectricity ranging from 10 to 60 min. After recovery with glucose, they were allowed to wake up and survive for 1 week. Control rats were recovered at the stage of EEG slowing. After sub-serial sectioning, the number and distribution of dying neurons was assessed in each brain region. Acid fuchsin was found to stain moribund neurons a brilliant red. Brains from control rats showed no dying neurons. From 10 to 60 min of cerebral isoelectricity, the number of dying neurons per brain correlated positively with the number of minutes of cerebral isoelectricity up to the maximum examined period of 60 min. Neuronal necrosis was found in the major brain regions vulnerable to several different insults. However, within each region the damage was not distributed as observed in ischemia. A superficial to deep gradient in the density of neuronal necrosis was seen in the cerebral cortex. More severe damage revealed a gradient in relation to the subjacent white matter as well. The caudatoputamen was involved more heavily near the white matter, and in more severely affected animals near the angle of the lateral ventricle. The hippocampus showed dense neuronal necrosis at the crest of the dentate gyrus and a gradient of increasing selective neuronal necrosis medially in CA1. The CA3 zone, while relatively resistant, showed neuronal necrosis in relation to the lateral ventricle in animals with hydrocephalus. Sharp demarcations between normal and damaged neuropil were found in the hippocampus. The periventricular amygdaloid nuclei showed damage closest to the lateral ventricles. The cerebellum was affected first near the foramina of Luschka, with damage occurring over the hemispheres in more severely affected animals. Purkinje cells were affected first, but basket cells were damaged as well. Rare necrotic neurons were seen in brain stem nuclei. The spinal cord showed necrosis of neurons in all areas of the gray matter. Infarction was not seen in this study. The possibility is discussed that a neurotoxic substance borne in the tissue fluid and cerebrospinal fluid (CSF) contributes to the pathogenesis of neuronal necrosis in hypoglycemic brain damage.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00688108
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  • 10
    Electronic Resource
    Electronic Resource
    Reply to the remarks by J. B. Brierley and A. W. Brown (1981)
    Springer
    Acta neuropathologica 55 (1981), S. 323-325 
    Details
    ISSN: 1432-0533
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00690997
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