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  • 1
    ISSN: 1432-1084
    Keywords: Magnetic resonance imaging ; Middle cerebral occlusion ; Brain oedema ; Cerebral infarct ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The development of ischaemic brain oedema caused by middle cerebral artery (MCA) occlusion was studied by serial magnetic resonance imaging (MRI) in rats. Multiple spin echo sequences were used with TR = 1500 ms and TE = 30–240 ms (8 echos). Subtraction images were obtained by subtracting the last three echos from the first echo. Fourteen rats were studied 3, 6, and 12 h and 1, 1.5, 3, 4, 6, and 8 days after MCA occlusion, and 2 of them also 3 and 6 weeks later. Two T2 components could be separated, a fast one representing bound water and a slow one representing free bulk water. MR showed T2 prolongation even on the first examination, and the highest values were observed 24h after occlusion. The subsequent examinations showed a slow reduction in oedema. MR studies 3 and 6 weeks after occlusion revealed an area of very long T2, which correlated well with infarction shown by histology. The subtraction images demonstrated both the infarct location and the oedematous changes in the surrounding uninfarcted tissue. MRI imaging employing T2 components and subtraction images appears to be a valuable method for observing the time course of the development and resolution of oedema in cerebral infarction.
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  • 2
    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.
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  • 3
    ISSN: 1432-0533
    Keywords: Adriamycin (Doxorubicin) ; Retrograde axonal transport ; Hypoglossal nucleus ; Neurotoxicity ; Mouse
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: 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.
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  • 4
    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.
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  • 5
    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.
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  • 6
    ISSN: 1432-0533
    Keywords: Neuron-specific enolase ; Human intestinal tract ; Immunocytochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Surgical specimens from various parts of the human intestinal tract as well as suction biopsy specimens, including mucosa and submucosa of the rectum, were fixed in formalin and embedded in paraffin by routine procedures. The distribution of immunoreactive areas indicating the presence of neuron-specific enolase (NSE) was then determined by using a sheep anti-human-NSE antiserum prepared in our laboratory. The immunocytochemical method revealed, in distinct contrast to other tissue components, the cell bodies of ganglion cells in the submucosa (Meissner's plexus) and in the muscle layers (Auerbach's plexus). The nerve bundles of the submucosa, of the muscle layers, and of the subserosal connective tissue were also stained, whereas the thin nerve processes of the mucosa were identified only rarely. The smooth muscle cells were stained weakly, but this reaction did not interfere with the identification of the neurons and their processes. Immunocytochemical demonstration of NSE is obviously a valuable additional method for visualization of the intrinsic intestinal innervation. It might well be that this technique will be of advantage in the diagnosis of pathologic processes such as those occurring in Hirschsprung's disease and allied conditions.
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  • 7
    ISSN: 1432-0533
    Keywords: Stroke-prone spontaneously hypertensive rats ; Blood-brain barrier ; Fibrinoid degeneration ; Brain edema
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The cerebrovascular lesions of severe chronic hypertension were studied by light microscopy in perfusion-fixed, subserially sectioned brains from stroke-prone spontaneously hyptertensive rats (SHRSP). The leakage and spread of plasma proteins were visualized by immunohistochemical detection of extravasated fibrinogen and by using an exogenous marker (Evans blue injected i.v.) for blood-brain barrier (BBB) dysfunction. In most SHRSP the hypertension did not lead to major BBB lesions in spite of a mean arterial pressure around 200 mm Hg at 6–9 months of age. Multifocal BBB damage occurred in a minor group of SHRSP, particularly within the cortex and the deep gray matter. A close spatial correlation was found between the leakage-spread of plasma constituents and the neuropathologic alterations. Fibrinoid degeneration of penetrating arterioles was found within the leakage sites. The surrounding gray matter showed petechial hemorrhages and abundant proteinaceous exudates rich in antifibrinogen-positive material. The current leakage of Evans blue and wide spread of fibrinoid substances suggested long-lasting damage to the BBB. Most neurons within the edematous gray matter had well preserved nuclei surrounded by a rim of cytoplasm with ill-defined outline as if vacuolation or lysis of the peripheral cytoplasm had occurred. The sponginess of the tissue progressed in severe cases to formation of necrotic cysts. Condensed acidophilic neurons were seen in the border zone between the edematous and more compact gray matter. The appearance and distribution of the gray matter lesions deviated in many respects from those commonly seen in regional ischemic infarcts. The fibrin thrombi found close to the cysts might be regarded as secondary events. The extensive spread of antifibrinogen-positive material within the white matter seemed to originate mainly from the chronic leakage sites in the gray matter. Increased number of large astrocytes were seen within the leakage sites and along the spreading pathways for the edema constituents. The white matter showed a rarefied texture with widely dispersed nerve fiber tracts, volume expansion, and occasional cyst formation. The results indicate a crucial pathophysiologic role for the egress, spread, and accumulation of vasogenic edema in the development of the cerebrovascular lesions in SHRSP.
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  • 8
    ISSN: 1432-0533
    Keywords: Propidium iodide ; Blood-brain barrier ; Circumventricular organs ; Fluorescence microscopy ; Perineurial permeability
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Propidium iodide, like its analogue ethidium bromide, is a compound which can be used as a marker of nucleic acids. This substance emits a red fluorescent light after exposure to UV light and has therefore been used previously as a nuclear stain in immunofluorescence studies and in flow cytometry. The present experiments were carried out to find out if propidium iodide could be traced in sections of the nervous system after i.v. injections. Due to the general toxicity of the compound detectable amounts of propidium iodide could not be obtained by a single i.v. injection. However, multiple injections of small amounts (0.1 mg) over a period from 15 min to 8 h (total dose 0.7–1.0 mg) were tolerated without any signs of adverse effects. In such experiments propidium iodide did not extravasate inot the cerebral gray or white matter, i.e., areas of the brain located within the blood-brain barrier (BBB). On the other hand, the compound spread into the choroid plexus, the circumventricular organs, the Gasserian ganglion, and sciatic nerve, i.e., regions located outside the BBB. It had a strong tendency to label the nucleus and the perikaryon of the cells in each of these territories. Perifascicular injection of propidium iodide around the sciatic nerve was followed by a marked cellular uptake not only in the epineurium but also in the endoneurium. The shape and position of the labeled nuclei strongly indicated that they were the nuclei of Schwann cells. Previous studies have shown that propidium iodide can be used as a retrograde tracer in neuroanatomic research. The compound, due to its fluorescent properties, appears to be useful for future studies in which one would like to influence the DNA contents in various cell populations of the nervous system. By using the retrograde axonal route groups of neurons could be influenced without causing primary injury to neighboring cells. By using the perifascicular mode of injection, the DNA content of Schwann cell nuclei can be influenced and the resulting effects investigated.
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  • 9
    ISSN: 1432-0533
    Keywords: Dentate ; Hypoglycemia ; Excitotoxin ; Dendrites ; Neuronal necrosis ; Membrane breaks ; Cerebrospinal fluid (CSF)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A detailed light- and electron-microscopic study of the damage to the rat dentate gyrus in hypoglycemia was undertaken, in view of the previously advanced hypothesis that hypoglycemic nerve cell injury is mediated by a released neurotoxin. The distribution of neuronal necrosis showed a relationship to the subarachnoid cisterns. Electron microscopy of the dentate granule cells and their apical dendrites revealed dendrosomal, axon-sparing neuronal pathology. Dentate granule cells were affected first in the dendrites in the outer layer of the stratum moleculare, sparing axons of passage and terminal boutons. Subsequently, the neuronal perikarya were affected, and Wallerian degeneration of axons followed. Cell membrane abnormalities preceded the appearance of mitochondrial flocculent densities and degradation of the cytoskeleton, and are suggested to be early lethal changes. The observed early dendrotoxic changes, and the dendrosomal, axon-sparing nature of the lesion implicate an excitotoxin-mediated neuronal necrosis in hypoglycemia.
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  • 10
    ISSN: 1432-0533
    Keywords: Hypertension ; Blood-brain barrier ; Immunohistochemistry ; Light microscopy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A transient increase in blood pressure was induced in 15 male Sprague Dawley rats by clamping the upper abdominal aorta for 8–10 min. Three rats served as controls. The brains were fixed by perfusion 2 h or 7 days later. Evan's blue-albumin (EBA) was used for macroscopic evaluation of the blood-brain barrier (BBB) integrity. Extravasated plasma albumin, fibrinogen and fibronectin were demonstrated by immunohistochemistry on paraffin sections. Glial fibrillary acidic protein (GFAP) was visualized in the same way. Parallel sections were analyzed for possible parenchymal changes associated with the BBB breakdown. Multiple focal areas of BBB opening were seen in the brains of the three rats killed 2 h after the hypertensive episode. The plasma proteins were present in the vascular wall, extracellular space and within certain neurons. Shrunken acid fuchsin positive neurons were seen in some areas of extravasation. After 7 days, in 5 out of 12 rats a few local lesions with EBA leakage and positive immunostaining for plasma proteins were seen. Structurally these lesions were characterized by shrinkage, fuchsinophilia and disintegration of neurons and proliferation of astrocytes. Thus, a transient opening of the BBB by acute hypertension may lead to permanent tissue damage.
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