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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 99 (2000), S. 496-502 
    ISSN: 1432-0533
    Keywords: Key words Glycogenosomes ; Mitochondria ; Aging rat ¶brain ; Visual pathway ; Retinal degeneration
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The significance of glycogenosomes (glycogen bodies), frequently seen in peripheral neurites of aging rats, is unknown and their occurrence elsewhere in nervous tissue is poorly documented. During the course of another study these bodies were observed by light microscopy in the visual pathways of aging rats where they have not previously been noted, and this report documents their occurrence, localisation and changes in density with age. Using the periodic acid-Schiff stain, small brightly red-staining bodies, digested by diastase and containing β-glycogen particles, were seen in increasing numbers in the neuropil of the superior colliculi in brain sections from animals of ¶5 months of age onwards. From 1 year until more than ¶2 years of age they steadily became more numerous in the outer one third of the superior colliculus, but remained small, rarely exceeding 4 μm. They were also found at later times in small numbers lying singly in the optic tract, the optic chiasm and optic nerves, although rarely in lateral geniculate nuclei. Similar bodies were also found to accumulate with age in the retinal photoreceptor cell layer. Changes in their densities and size with age in both regions have been documented and it is suggested that, while their occurrence in retinal photoreceptor cells may be due to sustained light damage leading to mitochondrial oxidative stress, it is difficult to implicate this mechanism for their occurrence in retino-tectal nerve fibres. The role of physical trauma, suggested for the presence of these bodies in aging peripheral axons, can be excluded and they appear not to be related to polyglucosan bodies.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 32 (1975), S. 115-125 
    ISSN: 1432-0533
    Keywords: Methyl Mercury ; Neurotoxicity ; Spinal Ganglia ; Cerebellar Cerebral Degeneration ; Vascular Permeability
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Young adult rabbits have been given methyl mercury salts by subcutaneous injections or by gastric intubation. After 3 daily doses of 7.5 mg/kg by the 8th day moderate to severe ataxia developed, and after 4 doses, severe ataxia. Some of these latter animals might die. This species, therefore, seems to be about twice as sensitive to the neurotoxic properties of methyl mercury salts as the laboratory rat. With the light microscope extensive degenerative changes were seen in primary sensory ganglion cells, in both Purkinje and granule cells of the cerebellum, and in certain cells in several regions of the forebrain. The earliest changes became visible microscopically about the fourth day after commencing dosing, and reached a maximum of severity from the 7th to 10th day. The pattern of neuronal damage more closely resembled that found in the cat and in man than that seen in the rat. No evidence of changed vascular permeability was detected.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 69 (1986), S. 295-308 
    ISSN: 1432-0533
    Keywords: Cisplatin ; Rat spinal ganglia ; Nucleolar segregation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Cisplatin given in doses of 0.5–2 mg to Wistar and to Sprague-Dawley rats produced nucleolar segregation of the dense fibrillar from the granular component in spinal root ganglion cells. The nucleolar segregation, found to the same extent in large and small neurons, was confirmed by specific silver staining and by electron microscopy. After repeated doses of 1 mg or 0.5 mg, up to 40% of affected nucleoli were observed by light microscopy. Focal clearing of the nucleoplasm of nuclei also occurred. Disorganisation of ribosomes was found in more severely intoxicated animals, especially in large light cells with shrinkage of the Nissl substance and apparent increase in neurofilaments, the latter occasionally distending the initial segment of the axon, but never extending further. Hypertrophy of the satellite cells with increase in the perineuronal intercellular spaces, often associated with irregular, scalloped nuclear and cell outlines, suggested that neuron shrinkage had occurred. This was confirmed by morphometry and marked alterations were found in nucleolar-to-nuclear and nucleolar-to-cell diameter ratios, nuclear and cell diameters were also somewhat reduced without change in the nucleus-to-cell ratios. Peripheral sensory nerve degeneration was not seen, and the animals died from non-neural causes. The probable role of these events in the production of sensory neuropathy is discussed.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 39 (1977), S. 81-88 
    ISSN: 1432-0533
    Keywords: Neuropathy in cats ; Thallium
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A method of poisoning cats with thallium is described. The chief functional disturbances in the nervous system are hypotonia and ataxia. The pathological changes are confined to the central and peripheral axons of primary sensory neurones and are of the ‘dying back’ type. No motor nerve fibre degeneration was found in this species. While extensive degeneration of sensory nerves was found, those in muscle were apparently unaffected. The significance of this anomalous finding is discussed in relation to the mechanism of the ‘dying back’ process.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 48 (1979), S. 1-9 
    ISSN: 1432-0533
    Keywords: Isoniazid ; Neuropathy ; Intoxication ; Axonal degeneration ; Ultrasfructure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Rats were given isoniazid either in a single large dose or continuously in drinking water and killed 5–105 days later. The distribution of degenerating fibres in various nerves (sensory and mixed) and in various sites along nerves and spinal roots was studied by light and electron microscopy. It was found that sensory nerves tended to be less affected than motor, and degeneration was more proximal in the latter. It was concluded that the pattern of degeneration and regeneration supported the view that the initial metabolic lesion is in the axon, rather than in the cell body.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 51 (1980), S. 169-177 
    ISSN: 1432-0533
    Keywords: “Dying back” ; Acrylamide ; Nerve ligature
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The application of a tight ligature around a nerve before daily administration of acrylamide (40 or 50 mg/kg) for 4 or 5 days leads to ascending degeneration of the injured nerves, the number of affected fibres and the degree of “dying back” being dependent on the dose of acrylamide given. The same response occurs whether acrylamide is given immediately after nerve ligation or 1 week later. Centripetal degeneration follows after a short delay period and is maximal at about 10 days after beginning acrylamide injections. The response is not found with INH, with misonidazole or with 2,5-hexanedione.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-0533
    Keywords: Purkinje Cells ; Selective loss ; Rat cerebellum ; Acrylamide ; β-Glucuronidase ; β-Galactosidase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Acrylamide (30mg/kg) given daily to rats five times each week for 3 weeks leads to progressive loss of Purkinje cells. The necrotic cells begin to be visible from the third day and their numbers reach a peak at the time when the dosing ceases at 18 days. They are less frequent thereafter, but are still visible almost 3 weeks later in small numbers. The density of Purkinje cells per millimeter falls to about 70% of normal at the 7th day, and a similar degree of reduction of the neuronal marker enzyme, β-galactosidase, is found over the same time scale. By contrast, while there is a brisk macrophage/microglial response in the molecular layer to the loss of the Purkinje cell dendrites, the increase in β-glucuronidase activity is relatively minor and is not significantly different from normal until after the 21st day. These responses are discussed in the context of the use of lysosomal enzyme activities in the assay of certain neurotoxic lesions.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 59 (1983), S. 216-224 
    ISSN: 1432-0533
    Keywords: Nerve crush ; PNS regeneration ; 2,5HD ; neurotilaments
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The pattern of recovery of myelinated axons in the posterior tibial nerve after crushing was studied in rats chronically intoxicated with 2,5-hexanedione. It was given for 2 weeks before curshing (200 mg/kg i.p. 5 times a week) or additionally for two further weeks after the nerve crush. Two animals were examined from each group at approximately, 1, 2, 3, 4, and 8 weeks later. Return of function in poisoned animals was slower than in the controls. The numbers of regenerating myelinated fibres was severely reduced in poisoned animals, up to 4 weeks later, but by 8 weeks the numbers equalled those in the control nerves. Marked impairment of initiation of neurite outgrowth was found, but once begun, axonal growth was comparable to controls and myelination occurred normally. Above the crush for 10 mm, filament-filled axonal swellings were found in poisoned animals accompanied by varying amounts of retrograde axonal degeneration. These findings are discussed in relation to the role of normal neurofilaments in axonal growth and the effects of probably cross-linking of these by 2,5-hexanedione on regnerating neurites.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1432-0533
    Keywords: Isoniazid ; Motor end plate ; Partial denervation ; Botulinum toxin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Chronic dosing of rats with isoniazid (INH) leads to an increase in the incidence of short “spontaneous” sprouts on motor end plates in the rat sternocostalis muscle. After partial denervation there is a slight increase in terminal sprouting after 1 week of dosing: this changes to a significant decrease from 2 to 6 weeks of dosing. The same is noted after local botulinum toxin injection, and in both conditions sprout length is significantly reduced. In vitro studies show that glutathione, cysteine and cystathionine all increase the incidence of short, “spontaneous” sprouts from end plates, while homocysteine and cystine have no effect. These findings are interpreted in the light of the hypothesis that in INH intoxication there may be a reduction of available axonal glutathione and cysteine due to inhibition of the pyridoxal phosphate-dependent enzymes cystathionine synthetase and cystathioninase.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1432-0533
    Keywords: Protein Incorporation ; Amino Acids ; p-Bromophenylacetylurea ; Neuropathy ; Neurotoxicity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The incorporationin vivo of14C-glycine into proteins has been studied during the period before and after the onset of neurotoxicity caused by an organic mercury compound and byp-bromophenylacetylurea in rats. The observations of Yoshinoet al. (1966) on the former intoxication have been confirmed in that an impairment of glycine incorporation into proteins was present in spinal ganglion cells, and may also be taking place in other tissues, before nerve fibre degeneration takes place. A similar reduction in amino acid incorporation into proteins during the period before the onset of paralysis due top-bromophenylacetylurea is found in spinal ganglia; this finding is confirmed by anin vitro method using14C-leucine as protein precursor.
    Type of Medium: Electronic Resource
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