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  • Electronic Resource  (14)
  • Botulinum A toxin  (4)
  • Spinal Cord  (4)
  • Acetylcholine  (3)
  • Permeability  (3)
Material
  • Electronic Resource  (14)
Keywords
  • 1
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Biochimica et Biophysica Acta (BBA)/Biomembranes 688 (1982), S. 486-494 
    ISSN: 0005-2736
    Keywords: (Erythrocyte) ; Amphotericin B ; Palytoxin ; Permeability
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Medicine , Physics
    Type of Medium: Electronic Resource
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  • 2
    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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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 267 (1970), S. 1-19 
    ISSN: 1432-1912
    Keywords: Tetanus Toxin-Labelled Protein ; Spinal Cord ; Pharmaco-kinetics ; Radioimmunassay ; Tetanustoxin ; Markierte Proteine ; Rückenmark ; Phar-makokinetik ; Radioimmunassay
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. The preparation and properties of125I-labelled tetanus toxin are described. 2. After intravenous injection there is a short phase when the labelled toxin is rapidly removed from the blood plasma. This initial period is followed by a slow second phase of decay which has a longer duration. The first phase in very pronounced in rabbits, but not in rats. Unlabelled toxin is removed equally fast from rabbit plasma, as has been revealed by measuring the immunological reactivity (so-called “junction test”) and toxicity. 3. Thirty minutes after i.v. administration torabbits about 2/3 of the radioactive label are found in the liver. The highest concentration is attained in the spleen. 24 hours later, the bulk of the label has been excreted in the urine and faeces, which indicates catabolism of the toxin. In therat, the concentration in the liver is much less prominent, and the excretion of the label is slower. In both species, the central nervous system does not accumulate more than just measurable quantities of the label, even if the animals are given large toxic doses. 4. After injection into the left gastrocnemius muscle of the rat, the labelled tetanus toxin is absorbed very slowly from the site of administration. It is taken up by the corresponding N. ischiadicus and the lumbar region of the spinal cord. The injection of toxin into the anterior leg leads to concentration of radioactivity in the cervical area of the medulla. The arrival of the label in the spinal cord coincides approximately with the appearance of local tetanus. Sectioning of the N. ischiadicus prevents the appearance of the local tetanus of the lower extremity. The enrichment of the toxin in the lumbar cord is prevented in operated, but not in sham-operated rats. 5. When the spinal cord was subdivided into four sectors, the label was found to be greatly concentrated in the ipsilateral ventral sector of the segment corresponding with the injected extremity. This indicates transport into the ventral roots. 6. 131I-labelled tetanus antitoxin also disappears very slowly from the rat gastrocnemius. In contrast to labelled tetanus toxin, however, it is not concentrated in the spinal cord.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 280 (1973), S. 177-182 
    ISSN: 1432-1912
    Keywords: Tetanus Toxin ; Iodine Labeling ; Spinal Cord ; Histoautoradiography
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 125I-labeled tetanus toxin was injected intravenously and intramuscularly in rats. Specific localisation within the spinal cord was obtained by histoautoradiography. 1. In generalized tetanus grain density was maximal in the ventral grey matter of spinal cord. The grains were closely correlated to the motoneurons and their neuropil. Other areas showed background activity only. 2. In local tetanus the injected side was labeled selectively. High grain density regularly covered a distinct group of motoneurons and their neuropil. 3. There is some evidence for intracellular accumulation of the toxin since the maximum of grain density was found over the perikarya whilst the nucleus corresponded to a minimum. 4. Cells yielding high grain density were less intensively stained with toluidine blue than neighbouring unlabeled cells. It is concluded from these experiments that tetanus toxin develops its action within or around selected motoneurons and that it induces morphological alterations there.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 272 (1972), S. 75-88 
    ISSN: 1432-1912
    Keywords: Tetanus Toxin ; Tetanus Antitoxin ; Local Tetanus ; Spinal Cord
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 0 1. Local tetanus was produced in rats by application of sublethal doses of 125I-tetanus toxin into the right m. gastrocnemius. Radioactivity was found in the lumbar part of the spinal cord for at least 24 days which is indicative of a long-lasting binding of toxin to its target organ. Radioactivity appears in the lumbar region before local tetanus becomes manifest. 2. The influence of antitoxin on both local tetanus and radioactivity of the lumbar cord heavily depends on the time of its application. When it is injected simultaneously into a foreleg, it prevents the symptoms and the spinal concentration process. When given ten hours after toxin, it does not change appreciably the severity of local tetanus; it diminishes, however, the radioactivity accumulating in the spinal cord. Antitoxin, given 48 hours after toxin, is ineffective in both respects. 3. 22 hours after application, about 9% of the initial radioactivity still persists in the injected leg; 50 hours after application, only 1–2% are still present. 4. Plasma radioactivity is measurable for between 50 and 96 hours in animals given 125I-toxin i.m. It is higher in animals having received antitoxin 10 hours after the toxin or simultaneously with toxin. 5. Labelled toxoid was prepared by formol treatment of labelled toxin. Following i.m. injection, toxoid was bound to a lesser degree and for a shorter time by the lumbar cord than was toxin. Like toxin, toxoid was found in the ipsilateral sciatic nerve, and simultaneous application of antitoxin prevented its appearance there as wells as in the lumbar cord. As with toxin, plasma radioactivity after injection of labelled toxoid was increased by simultaneous application of antitoxin into another leg. 6. It is concluded that antitoxin prevents the entrance of toxin into the spinal cord, but does neither remove nor detoxify appreciable amounts of radioactive material once fixed.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 303 (1978), S. 133-138 
    ISSN: 1432-1912
    Keywords: Tetanus ; Botulism ; Acetylcholine ; Nerve tissue ; Cell cultures
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Primary nerve cell cultures derived from embryonic rat central nervous system form [3H]ACh from exogenous [3H]Ch, and release it upon potassium depolarization. Pretreatment of the cultures with botulinum-A toxin or tetanus toxin diminishes the cellular accumulation of [3H]ACh. Poisoning the cultures during the period of [3H]Ch uptake fails to lower [3H]ACh formation. Dependent on dosage, both toxins suppress the release of [3H]ACh upon potassium depolarization. Heat-denaturated toxins as well as tetanus toxin preincubated with tetanus antitoxin were without effect.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 312 (1980), S. 255-263 
    ISSN: 1432-1912
    Keywords: Acetylcholine ; Tetanus toxin ; Botulinum toxin ; Myenteric plexus ; Transmitter release
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of tetanus and botulinum A toxin were studied on the electrically stimulated myenteric plexus-ileum strip of the guinea pig. The concentrations used were in the range of 104–106 mouse LD50/ml. 1. Tetanus and botulinu, A toxin slowly decrease the amplitude of the contractile response to field stimulation in a dose-dependent manner without influencing the sensitivity to acetylcholine of the smooth muscle. 2. Development of paralysis is preceded by a latent period. Washing and antitoxin slow the paralytic process only when applied during the latent period. 3. The time course of development of paralysis depends on the activity of the strip. It can be slowed by rest, high [Mg2+], or low [Ca2+], and accelerated by raising the stimulation frequency. 4. Substances like 4-aminopyridine, sea anemone toxin II and scorpion toxin which prolong the membrane depolarization restore temporarily the contraction of partially paralysed muscle strips. 5. Poisoned preparations do not differ from controls in their total acetylcholine contents, whereas formation as well as release of [3H]-acetylcholine are decreased by either toxin. It is concluded that a) tetanus toxin and botulinum A toxin are qualitatively indistinguishable with respect to their actions on the postganglionic cholinergic neurons in the ileum, botulinum A toxin being 5 times more potent than tetanus toxin, b) the effects of the toxins at postganglionic cholinergic neurons in the ileum and at motor nerve endings are qualitatively similar, botulinum A toxin being about 500 times more potent than tetanus toxin at the latter preparation (see Habermann et al., 1980b, c) both toxins influence the turnover of acetylcholine but not its tissue concentration.
    Type of Medium: Electronic Resource
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  • 8
    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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  • 9
    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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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 319 (1982), S. 101-107 
    ISSN: 1432-1912
    Keywords: Palytoxin ; Ouabain ; Erythrocytes ; Permeability ; ATPase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. Palytoxin in concentrations as low as 1 pM raises the potassium permeability of rat, human and sheep erythrocytes, and the sodium permeability of human erythrocytes. The release of potassium or sodium from human cells also occurs when extracellular sodium is replaced by choline. 2. Ouabain inhibits the release due to palytoxin of potassium ions from human, sheep and rat erythrocytes, and also the release of sodium ions from human cells. The glycoside effect is specific since a) it is already prominent with 5×10−8 M ouabain b) rat erythrocytes are less sensitive than human cells to ouabain c) potassium release due to amphotericin B or the Ca2+ ionophore A23187 is not influenced by ouabain and d) dog erythrocytes are resistant to palytoxin as well as to ouabain. 3. Palytoxin has no direct influence on the Na+, K+-ATPase. It inhibits the binding of [3H]ouabain to erythrocyte membranes within the same concentration range as unlabelled ouabain. It partially displaces bound [3H]ouabain, and partially inhibits the inactivation of erythrocyte ATPase by the glycoside. Depletion of ATP or of external Ca2+ renders the cells less sensitive to palytoxin. Nevertheless inhibition by ouabain can be still demonstrated with human cells whose ATP stores had been largely exhausted, and also in the absence of external Ca2+. 4. Palytoxin decreases the surface tension at the air-water interface. We assume that the formation of nonspecific pores by palytoxin is linked with its surface activity. Further experiments should demonstrate whether ouabain prevents the binding of palytoxin to erythrocytes (“receptor hypothesis”), or whether an ouabain-sensitive hydrolysis of trace amounts of ATP (“metabolic hypothesis”) promotes the palytoxin effect.
    Type of Medium: Electronic Resource
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