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  • 1
    Electronic Resource
    Electronic Resource
    Scanning electron microscopical study of the neurofibrillary tangles of Alzheimer’s disease (1997)
    Springer
    Acta neuropathologica 94 (1997), S. 78-86 
    Details
    ISSN: 1432-0533
    Keywords: Key words Paired helical filament ; Neurofibrillary ; tangles ; Scanning electron microscopy ; Alzheimer’s ; disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Neurofibrillary tangles (NFTs) have been ultrastructually studied by various methods, leading to several three-dimensional models of paired helical filaments (PHFs). In this study, we present the scanning electron microscopic findings of NFTs in an autopsy case of Alzheimer’s disease and clarify the three-dimensional structures of NFTs. NFTs were clearly defined in freeze-cracked nerve cells and consisted of two types of filamentous structures, straight and helical filaments. Straight filaments measured from 20 to 25 nm in diameter and had a smooth surface. They were slightly bent but mostly straight with no constrictions. One type of straight filaments ran in a bundle in the same direction, another was intertwined to each other. Most of the helical profiles of filaments usually measured about 28 nm in diameter, with a distance of 100 nm between periodic constrictions. They seemed to consist of a pair of isodiametric filaments of 10 nm in diameter. In addition, two unusual types of helical filaments were occasionally observed. One comprised thick filaments of about 38 nm in diameter, with a distance of 100 nm between constrictions; these helical filaments appeared to consist of two or more strands. The other comprised thin helical filaments of about 20 nm in diameter and regularly constricted at an interval of 50 nm. All types of the helical filaments examined in this case were leotropic. This result supports a protofilament model of PHFs. Scanning electron microscopy using the freeze-cracked and maceration method is a useful and simple method for three-dimensional observation of the filamentous structures in NFTs.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050675
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  • 2
    Electronic Resource
    Electronic Resource
    Scanning electron microscopical study of neurofibrillary tangles in a presenile patient with Down’s syndrome (1998)
    Springer
    Acta neuropathologica 96 (1998), S. 179-184 
    Details
    ISSN: 1432-0533
    Keywords: Key words Paired helical filaments ; Neurofibrillary ; tangles ; Down’s syndrome ; Alzheimer’s disease ; Scanning electron microscopy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract An autopsy case of a 64-year old woman with Down’s syndrome (DS) is reported with a special reference to the ultrastructure of neurofibrillary tangles (NFTs). NFTs and senile plaques were diffusely observed throughout the brain. The most severe changes were seen in the amygdaloid nuclear complex and hippocampus. Immunohistochemistry of the NFTs and senile plaques indicated the features identical to those in Alzheimer’s disease (AD). Ultrastructurally, NFTs were composed of straight filaments and two profiles of paired helical filaments (PHFs). By transmission electron microscopy, straight filaments measured 25–28 nm in diameter. As to the PHFs, one type was 33 nm in maximum diameter and constricted at a 75– to 80-nm interval. The other was 16–18 nm in maximum diameter and constricted at a 35– to 40-nm interval. By scanning electron microscopy, the diameter of the straight filaments measured up to 28–30 nm. Two profiles of PHFs were observed. One type of PHF showed thick filaments about 34 nm in maximum diameter and constrictions at an 80-nm interval. The other was about 17 nm in diameter and constricted at a 40-nm interval. The helical directions of both PHFs were left-handed. The frequency of PHFs with short interval was much higher in DS than AD. Furthermore, the length of the periodicity of this type of PHF was somewhat less than that of AD. Thus, these findings suggest that the neuropathological changes in DS and AD share a common etiopathology, but that some differences in the PHFs between DS and AD may reflect on molecular difference in the proteins or peptides associated with PHF formation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050879
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Blockade of voltage-sensitive sodium channels by NS-7, a novel neuroprotective compound, in the rat brain (1997)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 355 (1997), S. 601-608 
    Details
    ISSN: 1432-1912
    Keywords: Key words Neuroprotectant ; Voltage-sensitive sodium channel ; Batrachotoxin ; Saxitoxin ; Glutamate release ; Cerebral cortex ; Cardiac myocyte
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of 4-(4-fluorophenyl)-2-methyl-6-(5-piperidinopentyloxy) pyrimidine hydrochloride (NS-7), a novel neuroprotective compound, on the voltage-sensitive sodium channels (VSSC) were examined in the rat brain and cardiac myocytes. NS-7 inhibited [3H]batrachotoxinin A 20α-benzoate (BTX) binding (neurotoxin receptor site 2) in brain membranes with a Ki value of 1 μM , while the compound was less effective in the cardiac myocytes (Ki = 13 μM). Aconitine, on the other hand, inhibited [3H]BTX binding to brain membranes and cardiac myocytes with the same potency. In contrast, NS-7 had no affinity for [3H]saxitoxin binding in brain (neurotoxin receptor site 1). In superfused slices of the rat cerebral cortex, NS-7 inhibited the veratridine (5 μM)-evoked glutamate release in a concentration-dependent manner, the IC50 value of which was 7.7 μM, whereas the compound showed a weak and not significant suppression of KCl-evoked glutamate release. The tissue concentrations of NS-7 in the rat cerebral cortex and heart were 89 and 28 nmole/g tissue, respectively, 5 min after its intravenous injection (8 mg/kg). Furthermore, in the cerebral cortex, NS-7 distributed preferentially to the membrane-enriched synaptosomal fraction. Since neurotoxin receptor site 2 is located in the transmembrane region of the VSSC moiety, the channel function may be substantially inhibited by a peripheral administration of NS-7. These results suggest that the blockade of neurotoxin receptor site 2 of VSSC in the brain contributes to the neuroprotective action of NS-7.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00004990
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  • 4
    Electronic Resource
    Electronic Resource
    A novel Na+/Ca2+ channel blocker, NS-7, suppresses hypoxic injury in rat cerebrocortical slices (1998)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 358 (1998), S. 191-196 
    Details
    ISSN: 1432-1912
    Keywords: Key words Neuroprotectant ; Calcium channel blocker ; Sodium channel blocker ; Hypoxic injury ; ATP ; Cerebral cortex
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The substance 4-(4-fluorophenyl)-2-methyl-6-(5-piperidinopentyloxy) pyrimidine hydrochloride (NS-7) has been developed recently as a cerebroprotective compound with Na+ and Ca2+ channel blocking action. In the present study, the effect of NS-7 in an in vitro model of hypoxic injury was examined and the possible involvement of Na+ and Ca2+ channels in the hypoxic injury subsequently determined. When slices of rat cerebral cortex were exposed to hypoxia/glucose deprivation followed by reoxygenation and restoration of the glucose supply, marked leakage of lactate dehydrogenase (LDH) occurred 3–6 h after reoxygenation. This hypoxia/reoxygenation-induced injury was blocked almost completely by the removal of extracellular Ca2+ or by chelating intracellular Ca2+ with 1,2-bis(o-aminophenoxy)ethane-N,N,N’,N’-tetraacetic acid tetra(acetoxymethyl)ester (BAPTA/AM). In addition, combined treatment with the N-type Ca2+ channel blocker ω-conotoxin GVIA and the P/Q-type Ca2+ channel blocker ω-agatoxin IVA significantly reduced LDH leakage, although neither of these Ca2+ channel blockers alone, nor nimodipine, an L-type Ca2+ channel blocker, was effective. On the other hand, several Na+ channel blockers, including tetrodotoxin, local anaesthetics and antiepileptics, significantly reduced the hypoxic injury. NS-7 (3–30 µM) concentration-dependently inhibited LDH leakage caused by hypoxia/reoxygenation, but had no influence on the reduction of tissue ATP content and energy charge during hypoxia and glucose deprivation. It is suggested that blockade of Na+ and Ca2+ channels is implicated in the cerebroprotective action of NS-7.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00005242
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