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  • 1
    Electronic Resource
    Electronic Resource
    Cholera toxin B-subunit incorporation into synaptic vesicles of the neuromuscular junction of the rat (1986)
    Springer
    Cellular and molecular life sciences 42 (1986), S. 415-417 
    Details
    ISSN: 1420-9071
    Keywords: Synaptic vesicles ; endocytosis ; cholera toxin ; ganglioside ; neuromuscular junction ; rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary The B-subunit of cholera toxin, a nontoxic macromolecule which binds specifically to GM1 ganglioside, was conjugated to colloidal gold and injected into skeletal muscle of the rat. It was taken up rapidly in vesicles in the terminal axons at the neuromuscular junctions. Injection of albumin-colloidal gold conjugates resulted in an insignificant uptake. The results indicate that uptake of extracellular macromolecules into the terminal axon of the neuromuscular junction may be greatly enhanced by binding to gangliosides at the presynaptic membrane, and that it may occur without association with vesicular recycling related to transmitter release.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02118636
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  • 2
    Electronic Resource
    Electronic Resource
    Multiple mitochondrial DNA deletions in hereditary inclusion body myopathy (2000)
    Springer
    Acta neuropathologica 100 (2000), S. 23-28 
    Details
    ISSN: 1432-0533
    Keywords: Key words Hereditary inclusion body myopathy ; Mitochondria ; Mitochondrial DNA deletions ; Cytochrome c oxidase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We have recently described an autosomal dominant hereditary inclusion body myopathy (h-IBM). Clinically it is is characterized by congenital joint contractures and slowly progressive, proximal muscle weakness and ophthalmoplegia. There is deterioration of muscle function between 30 and 50 years of age. While young patients show minor pathological changes in muscle, the middle-aged and old patients show rimmed vacuoles and inclusions of filaments measuring 15–18 nm in diameter. Except for the absence of significant inflammation the histopathology is similar to that found in sporadic inclusion body myositis (s-IBM). In s-IBM mitochondrial alterations including cytochrome c oxidase (COX) -deficient muscle fibers are common. These are due to multiple mitochondrial DNA (mtDNA) deletions. In this study we investigated the occurrence of mitochondrial alterations in autosomal dominant h-IBM. Young affected individuals showed no mitochondrial changes but three patients aged 38, 51 and 59 years, respectively, showed ragged red fibers and COX-deficient muscle fibers. Polymerase chain reaction analysis showed multiple mtDNA deletions. By in situ hybridization clonal expansions of mtDNA with deletions were demonstrated in COX-deficient muscle fibers. Most of the analyzed deletion breakpoints showed nucleotide repeats flanking the deletions. The results show that COX-deficient muscle fibers and somatic mtDNA deletions are present in this family with h-IBM. The same factors may be involved in the development of mtDNA deletions in s-IBM and this family with h-IBM.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010051188
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  • 3
    Electronic Resource
    Electronic Resource
    Nerve fibre degeneration of the central and peripheral nervous systems in severe protein deprivation in rats (1981)
    Springer
    Acta neuropathologica 54 (1981), S. 121-127 
    Details
    ISSN: 1432-0533
    Keywords: Rat ; Protein deprivation ; Nerve fibre degeneration ; Central nervous system ; Peripheral nervous system
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Knowledge from previous reports that kwashiorkor in man may lead to nerve fibre degeneration prompted this study on rats. The rats were subjected to severe protein deprivation from 6 weeks of age. Protein deprivation was achieved by feeding the rats ad lib with a diet containing only 1.5% protein. Control rats received an iso-caloric diet with 14% protein. The vitamin content in both diets was well above normal requirements. In relation to body weight the protein-deprived rats did not consume less food than the control rats. Protein deprivation resulted in stunted body growth, markedly reduced values of serum albumin, and changes in the fur accompanied by areas of alopecia. Furthermore, the protein-deprived rats showed degeneration of nerve fibres in the medial parts of the posterior columns of the cervical but not the sacral part of the spinal cord and nerve fibre degeneration in the distal but not the proximal parts of the longitudinal tail nerves. Teased nerve fibre preparations of the tail nerves revealed changes consistent with the Wallerian type of degeneration. It is concluded that severe protein deprivation in young rats may lead to a “dying-back” type of neuropathy in the central and peripheral nervous systems.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00689404
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  • 4
    Electronic Resource
    Electronic Resource
    Effects of local extraneural application of diphtheria toxin on the sciatic nerves of normal and protein deprived rats (1979)
    Springer
    Acta neuropathologica 45 (1979), S. 141-145 
    Details
    ISSN: 1432-0533
    Keywords: Perineurium ; Protein deprivation ; Rat ; Peripheral nerve ; Diphtheria toxin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Diphtheria toxin was locally administered around the sciatic nerves of normal and protein deprived rats aged 3, 6, 12, and 26 weeks in order to investigate the permeability of the barriers enveloping the nerves. At all ages the rats developed a reversible hind limb paralysis linked to a severe segmental demyelination, indicating passage of the toxin into the endoneurium. From 6 weeks of age the pattern of reaction differed between the protein deprived and control rats. The differences are discussed and interpreted as being partly dependent on less efficient protective barriers of the sciatic nerves of the protein deprived rats.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00691892
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  • 5
    Electronic Resource
    Electronic Resource
    Barriers of peripheral nerve towards exogenous peroxidase in normal and protein deprived rats (1978)
    Springer
    Acta neuropathologica 43 (1978), S. 129-134 
    Details
    ISSN: 1432-0533
    Keywords: Protein deprivation ; Peripheral nerves ; Perineurium ; Macrophages ; Peroxidase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The protective barriers of the sciatic nerve in protein deprived and normal rats have been studied. Horseradish peroxidase (HRP) was applied extraneurally in rats aged between 4 and 26 weeks. The spread of the tracer was investigated 2 h, 24 h, and 3 days after application. Passage of tracer into the endoneurium was found in all rats but decreased with age. Within the endoneurium, HRP was phagocytized by normally occurring endoneurial histiocytes, which constitute part of the protective barrier system of peripheral nerves. The functional development of the nerve protective barriers was retarded in protein deprived rats. Observations made in this study support the concept of a transperineurial vesicular transport of macromolecules.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00685007
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  • 6
    Electronic Resource
    Electronic Resource
    Storage of lipofuscin in neurons in mucopolysaccharidosis (1981)
    Springer
    Acta neuropathologica 54 (1981), S. 287-292 
    Details
    ISSN: 1432-0533
    Keywords: Mucopolysaccharidoses III ; Sanfilippo's syndrome ; Histochemistry ; Electron microscopy ; Lipofuscin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A histochemical and ultrastructural study was made on the brain of a 23-year-old man with Sanfilippo's syndrome. In accordance with previous reports the cortical nerve cells contained a PAS-positive lipid storage substance. This showed intense autofluorescence in UV-light and was positive with various stains for lipofuscin. The storage material appeared ultrastructurally as inclusion bodies composed of short lamellated membranes, granular material, and vacuoles. In addition, concentrically and transversely lamellated membranous cytoplasmic bodies were observed in the nerve cells. It is concluded that the PAS-positive lipid storage material in the neurons was composed partly of lipofuscin in addition to other lipids presumably glycosphingolipids.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00697002
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  • 7
    Electronic Resource
    Electronic Resource
    Peripheral nerve fibre degeneration in protein-deprived young rats (1982)
    Springer
    Acta neuropathologica 57 (1982), S. 1-6 
    Details
    ISSN: 1432-0533
    Keywords: Rat ; Malnutrition ; Protein deprivation ; Peripheral nervous system ; Ultrastructure ; Degeneration
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In a previous study the occurrence of nerve fibre degeneration with a distribution as in dying-back neuropathies was described in young rats subjected to severe protein deprivation (Oldfors 1981). In this study the ultrastructural appearance of the degeneration of the nerve fibres at different levels of the longitudinal tail nerves in severely protein-deprived rats has been investigated. Various structural changes were noted, the most common being bands of Büngner indistinguishable from those seen in Wallerian degeneration. In nerve fibres which were less severely affected the most common finding was shrinkage of the axon with concomitant folding of the myelin sheath. Other structural changes included axonal accumulation of 10 nm filaments or mitochondria and other cell organelles, areas of demyelination, and projections of axolemma and Schwann cell membrane into the axon. Signs of axonal regeneration occurred but were infrequent. The degenerative changes seen at various levels of the nerves support the view that the neuropathy is of distal axonal type, but the structural appearance differs from several of the toxic dying-back neuropathies.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00688871
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  • 8
    Electronic Resource
    Electronic Resource
    Mitochondrial encephalomyopathy (1987)
    Springer
    Acta neuropathologica 74 (1987), S. 287-293 
    Details
    ISSN: 1432-0533
    Keywords: Mitochondrial encephalomyopathy ; Lactic acidosis ; Stroke-like episodes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We report the clinical and autopsy findings in a young man of 18 with a chronic progressive disorder comprised of lactic acidosis, mental deterioration, and epileptic seizures which were sometimes accompanied by stroke-like episodes with transient hemiparesis and cortical blindness. He died of congestive heart failure. The autopsy showed lesions of the gray matter of the brain. Both the putamen and parieto-occipital cortex showed loss of neurons and proliferation of macrophages, astrocytes and vessels. There was marked loss of neurons in the inferior olives, and slight reduction of the number of Purkinje cells. Skeletal muscle studies revealed ragged-red fibres and structurally abnormal mitochondria. The heart was enlarged: accumulations of mitochondria occurred in the muscle fibers. The liver exhibited marked fatty degeneration. Biochemical analyses showed normal activities of pyruvate dehydrogenase in thrombocytes, pyruvate carboxylase in lymphocytes, biotinidase in serum as well as succinate dehydrogenase and cytochrome c oxidase. The features of this disorder differ in many respects from cases of mitochondrial encephalomyopathy previously reported and cannot be assigned to any specific disease entity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00688194
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  • 9
    Electronic Resource
    Electronic Resource
    Cytochromec oxidase deficiency in infancy (1989)
    Springer
    Acta neuropathologica 77 (1989), S. 267-275 
    Details
    ISSN: 1432-0533
    Keywords: Mitochondrial myopathy ; Respiratory chain enzyme ; Enzyme-histochemistry ; Cytochromec oxidase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Five children with early onset of muscle weakness, lactic acidosis and deficient cytochromec oxidase staining in the muscle biopsy were studied. By oximetric assay of the respiratory chain of isolated mitochondria, cytochromec oxidase deficiency was confirmed in four of the cases, while one case showed only a slight decrease of cytochromec oxidase activity but considerably reduced activity when assayed spectrophotometrically. The muscle biopsies exhibited mitochondrial structural abnormalities and lipid storage in the four cases with oximetrically confirmed cytochromec oxidase deficiency, while the biopsy of the case with markedly reduced activity of cytochromec oxidase only in the enzyme-histochemical and spectrophotometrical assays had normal morphology. The light microscopical staining of cytochromec oxidase in the four cases with oximetrically confirmed deficiency showed deficient staining of the enzyme in all extrafusal fibres in three cases but one of the cases had normal enzyme-histochemical activity of cytochromec oxidase in about 25% of the fibres. In two cases muscle spindles were included in the biopsy. The intrafusal fibres showed normal enzyme-histochemical activity of cytochromec oxidase. Ultrastructural examination of the enzyme distribution in two of the cases revealed great heterogeneity of the mitochondria. The structurally abnormal mitochondria were usually deficient of enzyme activity. The mitochondria of endothelial cells appeared to have normal activity. Immunohistochemical staining with polyclonal antibodies to cytochromec oxidase revealed presence of immunoreactive material corresponding to the localisation of mitochondria in all cases. The results show that enzyme-histochemical staining of cytochromec oxidase is a useful technique to reveal deficiency of the enzyme and to study the distribution of the deficiency within the tissue both at the light microscopical and ultrastructural levels. However, the results of one of the cases show that deficiency revealed by the enzyme-histochemical technique is not completely reliable. Oximetric studies on isolated mitochondria are necessary to confirm the suspected deficiency and to reveal combined defects of the respiratory chain.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00687578
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  • 10
    Electronic Resource
    Electronic Resource
    Muscle regeneration (1989)
    Springer
    Acta neuropathologica 78 (1989), S. 264-269 
    Details
    ISSN: 1432-0533
    Keywords: Skeletal muscle ; Regeneration ; Growth factors ; Growth hormone ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Against the background of the importance of growth hormone (GH) for normal muscle growth, a study was performed to investigate whether lack of GH after hypophysectomy affects the cell proliferation and the local production of insulin-like growth factor-I (IGF-I) in the early stages of muscle regeneration in adult rats. The level of IGF-I in the serum of hypophysectomised rats was reduced to about 30% of that of controls. The incorporation of [methyl-3H]thymidine into the regenerating muscle showed a peak 6 days after the operation and then gradually declined to the end of the period of study 30 days after initiation of regeneration by ischemic necrosis. The DNA content rose to a maximum level after 6–8 days, and remained high after 30 days. There was no major difference in the incorporation of [3H]thymidine in regenerating muscle of hypophysectomised and control rats, but the DNA concentration in the regenerating muscles of hypophysectomised rats was significantly reduced after 30 days. There was a corresponding reduction in the number of nuclei per muscle fibre, indicating that hypophysectomy has a small effect on the cell proliferation during the early stages of muscle regeneration. Immunohistochemical demonstration of IGF-I in the regenerating muscle revealed the transient presence of immunoreactive material in satellite cells and myotubes after 6 to 8 days of regeneration but no immunoreactivity after 30 days. No obvious difference was observed between hypophysectomised and control rats, indicating that the endogenous production of IGF-I in regenerating skeletal muscle can occur independently of GH.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00687756
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