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  • 1
    Electronic Resource
    Electronic Resource
    A new syndrome of mental retardation and epilepsy characterized by dense microsphere accumulation (1991)
    Springer
    Acta neuropathologica 83 (1991), S. 92-94 
    Details
    ISSN: 1432-0533
    Keywords: Epilepsy ; Mental retardation ; Dense microsphere
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Dense microspheres (DMS) are enigmatic structures found within dendrites in the normal human cortex; their composition and function are unknown. We describe a case of a 29-year-old male with a history of mental retardation and epilepsy in whom the unique neuropathological finding was a marked excess of DMS, most notably in the neocortex. This is a previously undescribed neuropathological syndrome, and represents the first unequivocal association of DMS with a neurological disorder.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00294436
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    A new type of neuronal cytoplasmic inclusion: histological, ultrastructural, and immunocytochemical studies (1989)
    Springer
    Acta neuropathologica 77 (1989), S. 599-604 
    Details
    ISSN: 1432-0533
    Keywords: Neuronal inclusions ; Leigh disease ; Tropomyosin ; Actin ; Ultrastructure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A novel type of non-viral cytoplasmic inclusion is described, which was seen in virtually every neuron in the brain and spinal cord of a child with a presumed metabolic disorder whose clinical picture and CNS pathology were compatible with Leigh Syndrome. The ovoid to round inclusions were sharply demarcated, measuring up to 11 μm in diameter. They showed no distinctive staining with a battery of routine histological techniques. The ultrastructural features are unique, comprising non-membrane-bounded aggregates of randomly oriented plate-like structures with parallel linear densities depicting a periodicity of 11–16 nm. Immunocytochemical studies revealed strong staining with antisera to tropomyosin and weaker staining with antisera to actin. There was no reactivity with antibodies against neurofilaments, microtubules and their associated proteins, paired helical filaments, ubiquitin, vinculin or alpha-actinin. It is postulated that the metabolic disorder resulted in a neurodegenerative condition which manifested pathologically with lesions compatible with those of Leigh Syndrome. Associated with the condition was the discrete accumulation of cytoplasmic proteinaceous components, including tropomyosin, in the form of neuronal cytoplasmic inclusions possibly resulting from an alteration of the neuronal cytoskeleton.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00687887
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Chromogranin A inhibits dopamine release from rat striatal slices (1998)
    Springer
    Journal of neural transmission 105 (1998), S. 1083-1089 
    Details
    ISSN: 1435-1463
    Keywords: Keywords: Chromogranin A (CGA) ; striatal slices ; dopamine ; transmitter release ; calcium ; pancreastatin.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary. Chromogranin A (CGA), a prohormone and a protein component of endocrine and neural secretory granules, neuritic plaques in Alzheimer's disease and Lewy bodies in Parkinson's disease, inhibited the release of dopamine (DA) from perfused rat striatal slices. Dopamine release was stimulated by a pulse of high potassium (40 mM) medium introduced at 20 minutes (K1) and 55 minutes (K2) following equilibration. The ratio of K2/K1 was 0.80 ± 0.04 in control tissues, but fell significantly to 0.26 ± 0.08 when 100 nM purified CGA was added prior to the second potassium pulse. This reduction in DA release was equivalent to that seen when calcium was excluded from the buffer (0.19 ± 0.05). Pancreastatin, a centrally active peptide product of CGA, had no effect on stimulated DA release (0.77 ± 0.06), although it, as well as the other treatments, did reduce basal DA release. It is likely that the parent molecule itself, CGA, or an as yet unidentified product is responsible for inhibition of K-stimulated striatal DA release.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s007020050113
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    Paper (German National Licenses)
    Fulltext
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