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  • 1
    Electronic Resource
    Electronic Resource
    Neuropathological study on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine of the crab-eating monkey (1988)
    Springer
    Acta neuropathologica 75 (1988), S. 370-376 
    Details
    ISSN: 1432-0533
    Keywords: 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced parkinsonism ; Crab-eating monkey ; Substantia nigra ; Locus ceruleus ; Mitochondrial abnormalities
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Experimental parkinsonism was induced by systemic administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to the crab-eating monkey (Macaca fascicularis). In the acute stage, the substantia nigra showed necrotic nerve cells, extracellular release of pigment granules and histiocytic infiltration. The nerve cells underwent vacuolation of the cytoplasm with chromatin clumping of the nucleus and disintegration of the nucleolus. The striking feature was the presence of variously-shaped inclusion bodies within abnormal mitochondria which sometimes disclosed a distortion of the cristae. Golgi apparatus and endoplasmic reticulum were also dilated. In the locus ceruleus swollen nerve cells were observed with vacuolated cytoplasm and pyknotic nucleus where expanded mitochondria also contained the inclusions. Some of the inclusion bodies are probably insoluble precipitations due to inhibition of mitochondrial oxidation by a certain metabolite of MPTP. In the protracted stage the substantia nigra revealed a considerable loss of the nerve cells associated with melanophagia and astrocytic proliferation. A few surviving nerve cells showed an increased number of Golgi apparatus and rough endoplasmic reticula, and the presence of autophagosomes, dense bodies and intra-mitochondrial inclusions. These changes are interpreted as being a part of the reparative process from the cellular damage.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00687790
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  • 2
    Electronic Resource
    Electronic Resource
    Mitochondria covered with a net of parallel and latticed filaments in nigral neurons of monkeys with experimental parkinsonism (1989)
    Springer
    Acta neuropathologica 77 (1989), S. 489-493 
    Details
    ISSN: 1432-0533
    Keywords: Mitochondria ; Parkinson disease ; Substantia nigra ; 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) ; Monkey
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Nigral neurons of crab-eating monkeys treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) showed a peculiar configuration occasionally in mitochondria. The outer membrane of mitochondria was covered with a net of fine parallel or latticed filaments, which turned spirally about the long axis of the mitochondria. The filaments were approximately 8 nm in diameter: parallel filaments were arranged at intervals of about 13 nm from center to center; and latticed filaments intersected each other at an angle of almost 135°. When mitochondria were present in groups, the intermitochondrial gap was occasionally filled with the same parallel filaments. The netted mitochondria were frequently associated with intramitochondrial abnormalities such as small flocculent inclusions and disintegrated cristae. Only one or two netted mitochondria were counted in the perikaryon of one section of an injured neuron. They appeared in about one-third of mildly or moderately injured neurons in three of six MPTP-treated monkeys, and not in normal surviving and recovering neurons of treated animals, or in neurons of control animals. We consider the netted mitochondria to be a pathological configuration related to a metabolite of oxidation of MPTP, and to be different from the stubby mitochondria reported in amyotrophic lateral sclerosis (ALS) and a non-ALS case.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00687250
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  • 3
    Electronic Resource
    Electronic Resource
    Reappraisal of neurofibrillary tangles (1989)
    Springer
    Acta neuropathologica 77 (1989), S. 258-266 
    Details
    ISSN: 1432-0533
    Keywords: Neurofibrillary tangles ; Alzheimer's disease ; Pick bodies ; Immunohistochemistry ; Ultrastructure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We have studied the immunohistochemical reactivity and ultrastructure of both neurofibrillary tangles (NFTs) occurring with severe neurofibrillary diseases, and Pick bodies (PBs) associated with Pick's disease. The NFTs and PBs did not react immunohistochemically with the anti-nonphosphorylated neurofilament monoclonal antibody irrespective of whether they were pretreated with alkaline phosphatase. In granular neurons of the dentate fascia of Ammon's horn in cases of dementia of the Alzheimer type (DAT), NFTs either resembled PB-like inclusion bodies (Horoupian's inclusion bodies) in form, or had a perinuclear structure. Immunohistochemically and ultrastructurally, the NFTs in the dentate fascia in cases of DAT, including Horoupian's inclusion bodies, were similar to the NFTs in the pyramidal neurons of Ammon's horn, which are found most frequently in association with severe neurofibrillary diseases. Under a light microscope, Horoupian's inclusion bodies and PBs could not be differentiated and appeared to be argyrophilic round cytoplasmic inclusions in granular neurons of the dentate fascia. There were, however, ultrastructural differences. Horoupian's inclusion bodies consisted of bundles made up of straight tubules (STs), each about 15 nm in diameter. These bundles were intermixed with a few paired helical filaments which occurred at intervals of about 80 nm. On the other hand, PBs were composed of randomly distributed 15-nm-wide STs, intermixed with a very few fibrillary structures. These fibrils had a periodicity of about 160 nm, and ranged in width from about 15 nm to 30 nm. Horoupian's inclusion bodies associated with DAT and PBs associated with Pick's disease are different in this neuropathological aspect. The NFTs, including Horoupian's inclusion bodies in the dentate fascia in cases of DAT, are considered to be a manifestation of neurofibrillary degeneration.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00687577
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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