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  • Acetylcholine  (3)
  • Permeability  (3)
  • 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
    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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  • 3
    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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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 264 (1969), S. 476-493 
    ISSN: 1432-1912
    Keywords: Kinins ; Permeability ; Heat ; Inflammation ; Kinine ; Permeabilität ; Hitze ; Entzündung
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. The suboutis of rat paws heated (46,5° C) in situ has been perfused. Kinin activity could be demonstrated regularly in the fluid which was collected in ice. When the solutions were tested immediately after having passed the tissue, only some of the experiments yielded positive results. Native and125Jlabelled kininogen as well as kininogenase and kininase activities passed into the perfusates. The sensitivity to dextran and the kinin release on heating were, in contrast to recent reports, not correlated. 2. The release of the components of the kinin system approximately paralleled that of labelled human albumin. Their concentration rose until about 1 hour after the start of the heating. There was no priority of the components of the kinin system when compared with human albumin which can be regarded as permeability indicator. 3. Intravenously injected carboxypeptidase B, because of its lower molecular weight, entered the interstitial fluid more easily than did the plasma carboxypeptidase N. Its blood level decreased rapidly; but sufficient tissue concentrations could be maintained by intravenous infusions. Neither the volume nor the time dependence of the thermic edema changed during carboxypeptidase B-infusions. The same was true for infusions of trasylol, whereas phenylbutazone inhibited the edema significantly. Edema formed by short heating (30 sec, 55° C) was equally resistant to carboxypeptidase B. 4. In the skin and muscles of the heated rat paw, carbon particles mainly stained the capillary walls. This finding argues against a considerable involvement of “classical” mediators which should induce venular lesions. 5. Infusion of large amounts of bradykinin into the arterial supply did not imitate the thermic edema; neither has bradykinin been found in the perfusate of the subcutis. 6. In the light of these findings, a significant role of the kinin system in the thermic edema of the rat paw is to be doubted.
    Type of Medium: Electronic Resource
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  • 5
    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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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 316 (1981), S. 143-148 
    ISSN: 1432-1912
    Keywords: Tetanus toxin ; Botulinum toxin ; Acetylcholine ; Calcium ; Brain
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Slices or particles from rat forebrain cortex were preloaded with [3H]choline, and the release of [3H]acetylcholine was evoked with potassium ions in a superfusion system. Release depended on the presence of calcium. 1. Incubation of the preloaded tissue preparation for 2 h with tetanus or botulinum A toxin did not change the [3H]acetylcholine content or the ratio [3H]acetylcholine/[3H]choline. Tetanus toxin diminished, dependent on dose and time, the release of [3H]acetylcholine evoked by 25 mM K+. It was about ten times more potent than botulinum A toxin. The effect of botulinum toxin was due to its neurotoxin content. Raising the potassium concentration partially overcame the inhibition by the toxins. Hemicholinium-3, applied to preloaded slices, left the subsequent [3H]acetylcholine release unchanged. Pretreatment of particles with neuraminidase diminished the content of long-chain gangliosides to the detection limit. Such particles remained fully sensitive to tetanus toxin, and at least partially sensitive to botulinum A toxin. 2. The potassium or sea anemone toxin II stimulated uptake of 45Ca2+ into cortex synaptosomes or particles was not inhibited by either toxin. Both toxins appear to impede the Ca2+-dependent mobilization of an easily releasable acetylcholine pool, without inhibiting the transmembranal calcium fluxes.
    Type of Medium: Electronic Resource
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