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  • 1
    ISSN: 0014-5793
    Keywords: Botulinum A toxin ; Chain, heavy ; Chain, light ; Chromaffin cell, permeabilized ; Exocytosis
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 316 (1981), S. 135-142 
    ISSN: 1432-1912
    Keywords: Tetanus toxin ; Botulinum A toxin ; Choline ; Gangliosides ; Fixation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Tetanus toxin and, to a lesser degree, botulinum A toxin inhibit partially and noncompetitively the uptake of [3H]choline into a crude synaptosomal fraction from rat brain cortex. Botulinum toxin acts by its neurotoxin content. The effect is not due to nonspecific synaptosomal damage by the toxins as shown by the lactate dehydrogenase occlusion test, by the absence of swelling and by the preservation of choline stores. The ratio between [3H]acetylcholine and [3H]choline was decreased by both toxins. Inhibition by either toxin depends strongly on the temperature and duration of incubation, and is preceded by an initial latency period. The effect of tetanus toxin, once manifest, is largely resistant against antitoxin. It is not significantly diminished by pretreatment of the synaptosomes with V. cholerae neuraminidase. Fixation of 125I-tetanus toxin proceeds fast, is largely independent of temperature and is diminished by pretreatment of the synaptosomes with neuraminidase. Thus only some of the fixation sites, and not the long-chain gangliosides, are required for the effects of tetanus toxin. A slow, temperature-sensitive process links the fixation with the action. In contrast to rat synaptosomes the chicken preparation is more sensitive to botulinum A than to tetanus toxin, which reflects the differences in sensitivity between live birds and rodents. Our data underline the similarities between the effects of tetanus and those of botulinum A toxin. Their dependence on time and temperature, the time dependence of efficacy of antitoxin, and the concordance in species specificity indicate that the in vitro system mirros some crucial features of poisoning of isolated organs and live animals.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1912
    Keywords: Tetanus toxin ; Botulinum A toxin ; Neurotransmitter ; Uptake ; Release
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of tetanus toxin and botulinum A toxin on the uptake and evoked release of various neurotransmitters were studied using particles from rat forebrain, corpus striatum and spinal cord. 1. Uptake. Tetanus toxin partially inhibits the uptake of glycine and choline into spinal cord synaptosomes. The effect on glycine uptake becomes statistically significant after a lag period of 60\2-120 min. It is no longer present when the toxin is heated, antitoxin-treated or toxoided. The inhibition by botulinum A toxin of choline uptake into spinal cord synaptosomes is weak but measurable, that of glycine uptake is at the borderline of detection. The uptake of GABA into forebrain cortex synaptosomes is slightly inhibited by tetanus toxin but hardly by botulinum A toxin. The effects of tetanus toxin and botulinum A toxin on the uptake of noradrenaline into striatal synaptosomes are negligible. 2. Release. Tetanus toxin inhibits the potassium (25 mM) evoked release of radioactivity from rat forebrain cortex particles preloaded with labelled neurotransmitters. The sensitivity decreases in the following order: Glycine 〉 GABA \2〉 acetylcholine. The toxin also inhibits the release of radioactivity from striatal particles preloaded with labelled noradrenaline. It is always 10\2-50 times more potent on spinal cord than on brain particles. The sensitivity of the evoked release from the spinal cord decreases in the order glycine 〉 GABA 〉 acetylcholine 〉 noradrenaline. The toxin is identical with the causative agent because toxin-antitoxin complexes, toxoid and heated toxin do not influence the release from particles preloaded with glycine (spinal cord), GABA (forebrain) and noradrenaline (striatum). Botulinum toxin resembles tetanus toxin by its ability to diminish the release of radioactivity from preloaded forebrain (acetylcholine 〉 GABA), striatal (noradrenaline), or spinal cord (glycine) particles. The botulinum toxin effect on the striatum (noradrenaline) and on the spinal cord (glycine) is due to its neurotoxin content. The identity of the toxin and the causative agent has been established by preheating and preincubation with antitoxin. It is proposed that a) tetanus and, however to a much lesser degree, botulinum A toxin act in a basically similar manner on a process underlying the function of synapses in general, and b) the pronounced sensitivity of glycine and GABA release from spinal cord, together with the axonal ascent of tetanus toxin, may be crucial in the pathogenesis of tetanus.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 318 (1981), S. 105-111 
    ISSN: 1432-1912
    Keywords: Tetanus toxin ; Botulinum A toxin ; Noradrenaline outflow ; Gangliosides
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Tetanus toxin and, to a lesser degree, botulinum A toxin partially depress the basal and the potassium evoked outflow of [3H]noradrenaline from preloaded particulate rat forebrain cortex. The effect is due to the toxins and not to any contaminant, as shown by dialysis, heating and antitoxin treatment, and also by replacement of crystalline botulinum A toxin with purified neurotoxin. Tetanus toxin also depresses the outflow due to sea anemone toxin II, 4-aminopyridine and d-amphetamine. The effect of the toxins proceeds with time and strongly depends on temperature. Once manifest the tetanus toxin effect is not reversed by antitoxin. Pretreatment with V. cholerae neuraminidase degrades the long-chain gangliosides quantitatively to GM1. Tetanus toxin, applied subsequently remains fully active. High concentrations of tetanus toxin and botulinum A neurotoxin promote the outflow of small amounts of tritium within short incubation times. It is concluded: a) Tetanus toxin is a broad range neurotoxin which acts on processes subsequent to the depolarization step. b) Long-chain gangliosides are only binding sites, but not receptors of tetanus toxin. c) Botulinum A toxin is less potent but resembles tetanus toxin in both promoting and depressing the outflow of noradrenaline.
    Type of Medium: Electronic Resource
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