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  • 1
    Digitale Medien
    Digitale Medien
    Bicuculline-induced epileptic brain injury (1983)
    Springer
    Acta neuropathologica 62 (1983), S. 87-95 
    Details
    ISSN: 1432-0533
    Schlagwort(e): Status epilepticus ; Nerve cell injury ; Bicuculline ; Rat cerebral cortex
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: 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.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00684924
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  • 2
    Digitale Medien
    Digitale Medien
    Influence of systemic factors on experimental epileptic brain injury (1983)
    Springer
    Acta neuropathologica 60 (1983), S. 81-91 
    Details
    ISSN: 1432-0533
    Schlagwort(e): Brain injury ; Status epilepticus ; Hyperoxia ; Hypoxia ; Hypotension ; Vitamin E
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: 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.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00685351
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  • 3
    Digitale Medien
    Digitale Medien
    Cytofluorescence localization of adriamycin in the nervous system (1983)
    Springer
    Acta neuropathologica 60 (1983), S. 125-131 
    Details
    ISSN: 1432-0533
    Schlagwort(e): Adriamycin (Doxorubicin) ; Blood-nerve barrier ; Perineurium
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: 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.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00685356
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  • 4
    Digitale Medien
    Digitale Medien
    Pathogenesis of brain lesions caused by experimental epilepsy (1983)
    Springer
    Acta neuropathologica 59 (1983), S. 11-24 
    Details
    ISSN: 1432-0533
    Schlagwort(e): Status epilepticus ; Nerve cell injury ; Brain edema ; Rat hippocampal formation
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: 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.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00690312
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  • 5
    Digitale Medien
    Digitale Medien
    FITC-Dextrans as tracers for macromolecular movements in the nervous system (1983)
    Springer
    Acta neuropathologica 59 (1983), S. 53-62 
    Details
    ISSN: 1432-0533
    Schlagwort(e): Blood-brain barrier ; FITC-dextrans ; Vascular permeability ; Histotechnical procedure
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary A freeze-drying method has been developed by which fluorescein thiocarbamoyl dextrans (FITC-dextrans) can be localized in thin sections from nervous tissue and muscles. Labelled dextrans with molecular weights of 3,000, 20,000, 70,000 and 150,000 were injected intravenously (i.v.) into golden hamsters and samples from brain, trigeminal ganglia and sciatic nerves were examined 30 min or 4h later. For comparison experiments were also carried out in mice and some other tracers were tested as well. The dextrans did not pass out of blood vessels in cerebral cortex and white matter. The blood vessels in the trigeminus ganglion were permeable to all of the tested compounds, i.e. even the FITC-dextran with mol. wt. 150,000. Little, if any, i.v. injected dextran could be detected in the endoneurium of sciatic nerve fascicles. Even very high concentrations of dextrans (mol. wt. 3,000 and 150,000) injected around the sciatic nerves did not penetrate the perineurium of the sciatic nerve. As compared with other tracers dextrans have the advantage that they can be obtained in a wide range of molecular sizes. With the proposed technique presented at the end of this article they can be used for studies on vascular permeability in deep tissue like brain, ganglia and peripheral nerve. The use of these tracers will probably be particularly advantageous in investigations concerning the etiology of edematous conditions.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00690317
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  • 6
    Digitale Medien
    Digitale Medien
    Brain lactic acidosis and ischemic cell damage: Quantitative ultrastructural changes in capillaries of rat cerebral cortex (1983)
    Springer
    Acta neuropathologica 60 (1983), S. 232-240 
    Details
    ISSN: 1432-0533
    Schlagwort(e): Brain ; Incomplete ischemia ; Acidosis ; Capillaries ; Morphometry
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary Excessive tissue lactic acidosis has earlier been shown to aggravate structural damage of both neurons and glial cells in the rat cerebral cortex. To study the reactions of cortical capillaries, light- and electronmicroscopic morphometry was used. Rats were subjected to severe incomplete ischemia (cerebral blood flow below 5% of normal) for 30 min by clamping their carotid arteries and by lowering the blood pressure. Lactate production during ischemia was modified by preischemic administration of either saline (low lactic acidosis group) or glucose (high lactic acidosis group). In the animals with low lactic acidosis, only minimal vascular changes were seen after both 5 min and 90 min recirculation. In the high lactic acidosis group, the endothelial cells were swollen after 5 min of recirculation, and the changes grew markedly worse during 90 min of recirculation. Nuclear chromatin coarsened and mitochondria swelled up. Morphometry showed that the lumen narrowed as a result of endothelial swelling. In spite of variable degree of perivascular astrocytic edema, the outer capillary diameter was little changed in the experimental groups. It seems likely that endothelial swelling hampers postischemic circulation in incomplete ischemia accompanied by high lactic acidosis.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00691871
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  • 7
    Digitale Medien
    Digitale Medien
    Cytotoxic effects of adriamycin on mouse hypoglossal neurons following retrograde axonal transport from the tongue (1983)
    Springer
    Acta neuropathologica 61 (1983), S. 161-168 
    Details
    ISSN: 1432-0533
    Schlagwort(e): Adriamycin (Doxorubicin) ; Retrograde axonal transport ; Hypoglossal nucleus ; Neurotoxicity ; Mouse
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary We reported recently that the fluorescent, cytostatic drug, adriamycin (Doxorubicin) may reach the hypoglossal neurons by retrograde axonal transport from the nerve terminals of the tongue. The present investigation was undertaken to ascertain whether morphological changes occur in the hypoglossal neurons due to retrograde transport of adriamycin. Neuronal degeneration was observed in the hypoglossal nucleus 14 days after i.m. injection of adriamycin into the tongue. Early neuronal changes, such as rarefaction of the nuclear chromatin and segregation and fragmentation of the nucleolar components, were succeeded by cytoplasmic vacuolation, disappearance of ribosomes and other degenerative features. These observations are important from a neurotoxicologic viewpoint since they demonstrate that retrograde axonal transport may provide a route for the entry of adriamycin into the nervous system. Thus far, adriamycin appears to be the only known substance which can be traced directly in the neurons and cause their degeneration. An experimental method of damaging the motor neurons of the CNS has been introduced. A new toxic model for the investigation of experimental motor neuron disease is therefore available by the use of adriamycin.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00691980
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  • 8
    Digitale Medien
    Digitale Medien
    An improved Percoll density gradient for measurements of experimental brain edema (1983)
    Springer
    Acta neuropathologica 61 (1983), S. 201-206 
    Details
    ISSN: 1432-0533
    Schlagwort(e): Percoll ; Cerebral edema ; Density gradients
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary Microgravimetric methods are very useful for quantitative studies on brain edema. One of the techniques available is based on a gradient made up by NaCl and polyvinyl pyrrolidone-coated silica particles (Percoll). The present study was performed to find a way of minimizing fluid shifts between the gradient and the samples. For this purpose, five Percoll density gradients containing various concentrations of sucrose in isotonic saline were prepared. Equivalent samples of normal mouse brain were then added and their second slow movement (drift) indicating interactions between the tissue and the gradient was followed. A concentration of 0.125 M sucrose eliminated the drift of the samples almost entirely. The capacity of this sucrose-containing gradient to reveal brain edema was then evaluated by comparing the density values obtained with those measured in the traditional bromobenzene-kerosene gradient as described by Nelson et al. (1971). For this purpose, we produced in the mouse an acute cytotoxic edema by triethyltin intoxication and a vasogenic edema by a cortical cryogenic injury. The two gradients showed almost identical results. We conclude, therefore, that the 0.125 M sucrose-containing Percoll gradient is a very good alternative to bromobenzene-kerosene gradients used for brain density determinations. Furthermore, Percoll gradients are very stable and contain only non-toxic ingredients.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00691986
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  • 9
    Digitale Medien
    Digitale Medien
    Toxic effects of adriamycin on the central nervous system (1983)
    Springer
    Acta neuropathologica 61 (1983), S. 291-299 
    Details
    ISSN: 1432-0533
    Schlagwort(e): Adriamycin ; Doxorubicin ; Neurotoxicity ; Blood-brain barrier ; Circumventricular organs
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary Recent experimental studies have shown that the cytotoxic antibiotic adriamycin (doxorubicin) after systemic administration can enter the so-called circumventricular organs (CVO) of the brain of the mouse. The present experiments were performed to find out whether such penetration of the brain is associated with signs of neurotoxic injury. For this purpose, light-and electron-microscopic observations were carried out on three of these organs: the neurohypophysis (NH), median eminence (ME), and postremal area (PA). Pronounced widening of the extracellular space indicating the presence of edema was present in all the regions, particulary in animals examined within 3 days of injection of the drug. Many degenerated axon terminals were observed in the NH and ME. The glial cells within these regions showed rarefaction of the nuclear chromatin, nucleolar segregation, and also cytoplasmic changes. The PA presented marked cellular changes resulting in degeneration of neurons, which was most evident 30 days after the injection. Hence, regions of the CNS outside the blood-brain barrier can be reached by adriamycin after systemic administration, and the drug can induce morphological changes there. The doses of the drug used in the present experiments were comparable to those given to patients for the treatment of malignant tumors.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00692000
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