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  • 1
    Electronic Resource
    Electronic Resource
    The sternocleidomastoid test: an in vivo assay to investigate botulinum toxin antibody formation in humans (2000)
    Springer
    Journal of neurology 247 (2000), S. 630-632 
    Details
    ISSN: 1432-1459
    Keywords: Key words Botulinum toxin therapy ; Therapy failure ; Antibodies ; Electromyography
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In a small number of patients treated with botulinum toxin (BT) antibody (Ab) formation occurs. Bt Ab can be detected by the mouse protection assay (MPA) or by the mouse diaphragm assay (MDA). Both methods, however, have major drawbacks. We tested a method for detecting BT Ab which measures the BT-induced reduction in the electromyographic amplitude of the mean maximal voluntary activation (M-EMG) of the sternocleidomastoid muscle. The M-EMG reduction was compared in 17 patients with cervical dystonia and secondary BT therapy failure to the M-EMG reduction previously measured in controls. Values more than 2 SD below the mean of controls were considered abnormal. Six patients showed BT Ab on the MPA and MDA; all of these had abnormal M-EMG reductions. Eleven patients showed no BT Ab on MPA and MDA testing; in ten of these the M-EMG reduction was normal, and in one it was pathological, but MDA testing later changed to positive under continued BT therapy. The sternocleidomastoid test is easy to perform and produces quantitative results. Since its sensitivity and specificity are at least as good as those of the MDA and the MPA, it can replace them.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004150070132
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  • 2
    Electronic Resource
    Electronic Resource
    Microelectrode measurement of cell membrane potential in isolated hepatocytes attached to collagen
    Amsterdam : Elsevier
    Biochimica et Biophysica Acta (BBA)/Biomembranes 863 (1986), S. 318-324 
    Details
    ISSN: 0005-2736
    Keywords: (Hepatocyte) ; K^+ channel ; Membrane potential ; Microelectrode ; Ouabain
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Medicine , Physics
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0005-2736(86)90274-9
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  • 3
    Electronic Resource
    Electronic Resource
    KINETICS OF [3H]ACETYLCHOLINE SYNTHESIS AND RELEASE IN PRIMARY CELL CULTURES FROM MAMMALIAN CNS (1978)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 30 (1978), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract— The present study was undertaken to characterize the cholinergic system of primary cell cultures of mouse and rat CNS.In confirmation of previous reports, primary cultures were found to contain choline acetyltransferase (ChAc). Furthermore they contain acetylcholine (ACh) as measured by two different bioassays. They also synthesize [3H]ACh from [3H]Choline offered to the cultures.The formation of [3H]ACh is inhibited in the presence of hemicholinium-3 (10−6m) to 50% or ouabain (10−3m) to 20% of the values found in untreated cultures. Omission of Na + from the incubation solution also diminishes the [3H]ACh formation of the cells.[3H]ACh is released upon depolarisation by K+ ions in a concentration dependent manner. The release can be prevented by lack of Ca2+ ions in the incubation solution.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1978.tb10796.x
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  • 4
    Electronic Resource
    Electronic Resource
    Suppression of 3H-acetylcholine release from primary nerve cell cultures by tetanus and botulinum-A toxin (1978)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 303 (1978), S. 133-138 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF00508058
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  • 5
    Electronic Resource
    Electronic Resource
    Inhibition of synaptosomal choline uptake by tetanus and botulinum a toxin (1981)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 316 (1981), S. 135-142 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF00505307
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  • 6
    Electronic Resource
    Electronic Resource
    Distinct targets for tetanus and botulinum A neurotoxins within the signal transducing pathway in chromaffin cells (1991)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 344 (1991), S. 387-395 
    Details
    ISSN: 1432-1912
    Keywords: α-Toxin ; Proteinkinase C ; Exocytosis ; G-Proteins ; Cyclic nucleotides
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Tetanus and botulinum A neurotoxins inhibited exocytosis evolved by various secretagogues in intact and permeabilized chromaffin cells. The block of exocytosis in intact chromaffm cells due to botulinum A neurotoxin could partially be overcome by enhancing nicotine- and veratridine-induced stimulation, whereas the block due to tetanus toxin persisted under the same conditions. The receptor-mediated restoration of 3H-noradrenaline release was specific for nicotinic stimulation, because exocytosis did not occur during muscarinic stimulation. Depolarization of intact chromaffin cells with increasing concentration of K+ failed to restore exocytosis that had been blocked by either toxin. When chromaffin cells, treated with tetanus or botulinum A neurotoxins, were exposed to the Ca2+-ionophore A 23187 or permeabilized by staphylococcal α-toxin, Ca2+-stimulated exocytosis was also inhibited. The inhibition was unaffected by increasing concentrations of free Ca2+. Activation of proteinkinase C and of G-proteins by phorbolester and GMPPNHP, respectively, increased Ca2+-induced exocytosis in control cells as well as in cells treated with tetanus and botulinum A neurotoxins. The block, however, could not be relieved by these manipulations, and it could not be relieved by activating the cGMP or cAMP pathways with analoga of cyclic nucleotides, phosphodiesterases inhibitors, and forskolin either. It is concluded that nicotine and veratridine trigger a mechanism within the sequence of events leading to exocytosis that is located beyond the increase in intracellular Ca2+-concentration. This pathway may not be affected by botulinum A neurotoxin. The target of tetanus toxin is probably located even closer to the fusion process, i. e. beyond the step upon which botulinum A neurotoxin acts.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00172577
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  • 7
    Electronic Resource
    Electronic Resource
    Blockade by tetanus and botulinum A toxin of postganglionic cholinergic nerve endings in the myenteric plexus (1980)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 312 (1980), S. 255-263 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF00499155
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  • 8
    Electronic Resource
    Electronic Resource
    Tetanus toxin and botulinum A toxin inhibit release and uptake of various transmitters, as studied with particulate preparations from rat brain and spinal cord (1981)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 316 (1981), S. 244-251 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF00505657
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  • 9
    Electronic Resource
    Electronic Resource
    Tetanus toxin and botulinum a toxin inhibit acetylcholine release from but not calcium uptake into brain tissue (1981)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 316 (1981), S. 143-148 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF00505308
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  • 10
    Electronic Resource
    Electronic Resource
    Tetanus toxin blocks the neuromuscular transmission in vitro like botulinum a toxin (1980)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 311 (1980), S. 33-40 
    Details
    ISSN: 1432-1912
    Keywords: Tetanus toxin ; Botulinum toxin ; Neuromuscular junction ; Calcium ; Neuraminidase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. The blocking effect of tetanus toxin on the neuromuscular junction of the mouse phrenic nervehemidiaphragm preparation exposed to the toxin (0.05–20 μg/ml) in the organ bath was studied and compared with the action of botulinum A toxin. 2. The time course of the paralysis of the diaphragm could be divided into a latent and a manifest period. Still during the latent period the effect of the toxin became progressively resistant to washing and, with some delay, to antitoxin. 3. Between 25 and 41°C the time until paralysis strongly depended on temperature with Q 10 of about 2.7. 4. Procedures increasing the transmitter release shortened, and procedures depressing it prolonged the time until paralysis. 5. 4-Aminopyridine and guanidine temporarily restored the contraction of the partially paralyzed diaphragm, indicating the persistence of activatable calcium and acetylcholine pools. Raising the external Ca2+-concentration and application of the Ca-Ionophore A 23187 were ineffective in the doses applied. 6. About 80 min after exposure to the toxin (10 μg/ml), the m.e.p.p. activity decreased by a factor of 30. Parallel to this, paralysis of nerve evoked muscle contraction developed. 7. Neuraminidase treatment did not prevent tetanus toxin poisoning. 8. The paralysis is produced by tetanus toxin itself and not by contaminants as shown by the parallel decrease of toxicity and paralysis following treatment with either antitoxin or brain homogenate, or by the use of spontaneously inactivated toxin. 9. Tetanus toxin was compared with botulinum A toxin as to the shape of its dose-response curve, time course of paralysis, temporary reversal by 4-aminopyridine and behaviour against Ca-ionophore. In any case, both toxins were indistinguishable, albeit botulinum A neurotoxin was calculated to be about 2000 times more potent than tetanus toxin.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00500299
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