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  • 1975-1979  (4)
  • 1970-1974
  • 1979  (4)
  • 1
    Electronic Resource
    Electronic Resource
    Investigations on the mechanism of cyclic guanosine monophosphate increase due to depolarizing agents as studied with sea anemone toxin II in mouse cerebellar slices (1979)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 307 (1979), S. 159-166 
    Details
    ISSN: 1432-1912
    Keywords: Sodium channel ; Calcium ; Cyclic GMP ; Cerebellum
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Sea anemone toxin II (ATX II) and MCD-peptide, like other depolarizing agents, raise the content of cGMP and to a lesser extent of cAMP in mouse cerebellar slices. Na+ influx and Ca2+ movement are involved in their mode of action, as indicated by the following observations: 1. The rise of cGMP due to ATX II, MCD-peptide and high potassium was diminished when Na+ had been replaced by Li+. 2. The effects of both toxins and veratridine, but not of high potassium stimulation were prevented by tetrodotoxin (TTX). 3. The cGMP accumulation due to both toxins was abolished in the absence of extracellular Ca2+. 4. The so-called Ca2+-antagonist (−)-D-600 blocked the increase of cGMP due to ATX II, MCD-peptide, veratridine and high potassium. 5. ATX II stimulated the 45Ca2+ uptake in mouse cerebellar slices which was prevented by TTX and (−)-D-600.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00498458
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Iodine labelling of sea anemone toxin II, and binding to normal and denervated diaphragm (1979)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 309 (1979), S. 165-170 
    Details
    ISSN: 1432-1912
    Keywords: Sea anemone toxin ; Sodium channels ; Intraventricular injection ; Surface activity ; Peptide labelling
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. Sea anemone toxin II (ATX II) which keeps the activated sodium channels open, can be labelled at its histidine residues with 125I up to a specific radioactivity of 500 Ci/mmole. Upon intraventricular injection in mice, ATX II causes acute, short-lasting hyperexcitation and convulsions. Its LD50 in mice is between 25 and 50 ng of the native peptide, and between 50 and 100 ng of the radioactive material per animal. 2. The labelled peptide is bound to mouse diaphragm from where it can be displaced by ATX II and, even better, by scorpion neurotoxin but not by other basic peptides, e.g., histone or aprotinin. Binding is not significantly influenced by 50 mM potassium, by replacing sodium with choline, by veratridine or tetrodotoxin. In contrast to binding of α-bungarotoxin, binding of ATX II is not changed by denervation of the diaphragm. ATX II binds not only to the muscular but also to the tendinous moiety of the mouse diaphragm. 3. ATX II lowers the surface tension of water. Further experiments are needed to establish the usefulness of 125I-ATX for labelling sodium channels in excitable membranes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00501225
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Effects of ion channel toxins and specific neurotoxins on the cyclic nucleotide content of cerebellar slices, primary brain cultures and neural cell lines (1979)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 307 (1979), S. 151-157 
    Details
    ISSN: 1432-1912
    Keywords: Cyclic nucleotides ; Neurotoxins ; Sodium channel ; Neural tissue
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary cAMP and cGMP were measured in mouse cerebellar slices, neural cell lines and primary nerve cell cultures from rats after treatment with different neurotoxins and high potassium. 1. Sea anemone toxin II (ATX II), which is known to keep the activated sodium channels open, raised the cGMP content of mouse cerebellar slices up to 35-fold and doubled their cAMP content. Mast-cell-degranulating peptide (MCD-peptide) from been venom increased cGMP levels up to 15-fold. The effects of both toxins on the cyclic nucleotide content were mimicked by depolarizing agents, like high potassium and veratridine. Primary nerve cell cultures (4 weeks old) responded to ATX II and high potassium with an increase of both cGMP and cAMP, however to a smaller extent as compared with slices. Excitable structures appear to be relevant, because younger cultures (2 weeks and less) and several neural cell lines did not respond to ATX II. 2. Specific neurotoxins like tetanus toxin, botulinum A toxin and apamin from bee venom had no effect on the cyclic nucleotide content of cerebellar slices and of primary nerve cell cultures. In cerebellar slices the potassium-stimulated increase of cAMP and cGMP was not affected by previous exposure of the slices to tetanus toxin or apamin. We conclude that opening of sodium channels in excitable membranes generally raises the cyclic nucleotide content whereas the mode of action of specific neurotoxins is not reflected by changes in the overall content of cyclic nucleotides.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00498457
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    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Normal and pseudorabies virus infected primary nerve cell cultures in scanning electron microscopy (1979)
    Springer
    Medical microbiology and immunology 167 (1979), S. 117-126 
    Details
    ISSN: 1432-1831
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Primary cell cultures from the central nervous system of the embryonic rat were inoculated with pseudorabies virus. Their morphological changes were studied by phase contrast microscopy and by scanning as well as by transmission electron microscopy. Uninfected cultures display two distinct cell layers in scanning electron microscopy: a flat continuous monolayer supports a heterogeneous population of individual, presumably neural cells, which emit processes of different number and size. The latter cells form contacts by a dense network of fibres. Infectious virus is propagated in these nerve cell cultures with similar effectivity as in other cultures. The infection leads to fusion and death of the cells. By the time the cytopathic effect is visible, nearly all cells, including those of neuronal and those of nonneuronal appearance, are studded with ample amounts of virus-sized particles. The particles represent viruses as demonstrated by transmission electron microscopy or by treatment with a hyperimmune serum directed against pseudorabies virus structural components. Hyperimmune serum leads to clustering of the particles at the cell surface. The amount of virus particles per surface unit was about 10 times higher on neural cells as compared to primary rabbit kidney cells. The concentration of infectious particles in the supernatant, however was approximately the same. The system described appears to be useful for the study of acute virus effects on neural tissue under strictly controlled conditions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02123561
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    Paper (German National Licenses)
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