Die Wirkung von Skorpiongift auf die Ionenstr�me des Ranvierschen Schn�rrings

Koppenhöfer, E; Schmidt, Hans

doi:10.1007/bf00592631

Cited by 129 publications

(16 citation statements)

References 17 publications

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“…We have tested the effects of two agents known to slow or remove fast inactivation of sodium channels, namely internal iodate ions (Staimpfli, 1974;Neumcke, Schwarz & StAmpfli, 1980 Koppenh6fer & Schmidt, 1968;Conti, Hille, Neumcke, Nonner & Stimpfli, 1976;Wang & Strichartz, 1983).…”

Section: Chemically Modified Sodium Channelsmentioning

confidence: 99%

Multiple kinetic components of sodium channel inactivation in rabbit Schwann cells.

Howe

Ritchie

1992

The Journal of Physiology

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SUMMARY1. We have studied the kinetics of inactivation of sodium currents evoked in Schwann cells from neonatal and adult rabbits with patch-clamp recording techniques. The decay both of whole-cell currents and of ensemble currents obtained from outside-out patches was reasonably well-described by single exponential fits which gave values for the time constant, Th, similar to those found for such currents in nerve (about 0-5 ms at 0 mV). Although inclusion of an additional exponential component usually improved the fits to the decay of these currents, the relative amplitude of the slower component (time constant 3-6 ms) was always small.2. The time course of recovery from steady-state inactivation clearly consisted of two exponential components. At -120 mV, recovery from steady-state inactivation at -50 mV consisted of a fast component with a time constant of 2-2 + 02 ms and a much slower component with a time constant of 12 + 02 s (n = 9). The relative amplitude of the slow component (expressed as a fraction of the sodium current when inactivation was removed completely) was 0-56 + 0 03. The corresponding amplitudes of the slow component when similar experiments were done from holding potentials of 0 and -70 mV were 0-80 + 0-04 and 0-36 + 0-03, respectively (n = 5 and 8).3. The onset of steady-state inactivation also followed a bi-exponential time course. The time constant of the slower component was similar at each potential examined (0, -50 and -70 mV), being 6-7 s. The relative amplitude of the slow component of onset depended on membrane potential, and it was similar (at each potential examined) to the corresponding amplitude of the slow component of recovery.4. The inclusion of 40 mM-iodate ions in the pipette solution slowed the decay of whole-cell sodium currents, as did the extracellular application of venom (10 jug ml-') from the scorpion Leiurus quinquestriatus. Prolonged exposure of the cells to Leiurus venom appeared to increase the steady-state amount of slow inactivation. 5. Records of single-channel sodium currents tended to cluster into records which either did, or did not, contain openings. This apparently non-random behaviour depended on membrane potential, and on the frequency at which the test steps were repeated, in the way expected if it resulted from slow inactivation.6. The results indicate that sodium channels in Schwann cells can exist in at least three different inactivated states and provide further evidence of the similarity between these sodium channels and sodium channels in excitable cells.MS 9300

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Section: Chemically Modified Sodium Channelsmentioning

confidence: 99%

Multiple kinetic components of sodium channel inactivation in rabbit Schwann cells.

Howe

Ritchie

1992

The Journal of Physiology

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“…The sea anemone toxin effect is antagonized by tetrodotoxin. Neurotoxins are essential tools for the analysis of molecular aspects of nerve conduction and transmission. Toxic molecules already available for study of molecular aspects of conduction include: (i) tetrodotoxin and saxitoxin, which are highly specific for blocking the Na+ channel in most axons (1,2); (ii) veratridine and batrachotoxin, which depolarize nerve membrane by a selective increase in the resting sodium permeability (2-5); and (iii) scorpion neurotoxin, a miniprotein which affects reversibly the closing of the Na+ channel and the opening of the K+ channel (6)(7)(8).…”

Section: Introductionmentioning

confidence: 99%

Sea anemone toxin:a tool to study molecular mechanisms of nerve conduction and excitation-secretion coupling.

Romey¹,

Abita²,

Schweitz³

et al. 1976

Proc. Natl. Acad. Sci. U.S.A.

163

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The effects of a polypeptide neurotoxin from Anemonia sulcata on nerve conduction in crayfish giant axons and on frog myelinated fibers have been analyzed. The main features of toxin action are the following: (i) the toxin acts at very low doses and its action is apparently irreversible. (il) The toxin selectively affects the closing (inactivation) of the Na+ channel by slowing it down considerably; it does not alter the opening mechanism of the Na+ channel or the steady-state potassium conductance. (iii) The tetrodotoxin-receptor association is unaffected by previous treatment of the axonal membrane with the sea anemone toxin. (iv) Conversely, the sea anemone toxin can only associate with the membrane when the Na+ channel is o en for Na+; it does not bind when the channel is previously blocked by tetrodotoxin. (v) Besides its effect on the action potential, the sea anemone toxin displays a veratridinetype depolarizing action at low Ca2+ concentration which can be suppressed by tetrodotoxin. The sea anemone toxin greatly stimulates the release of {Y43H]aminobutyric acid from neurotransmitter-loaded rat brain synaptosomes. The apparent dissociation constant of the neurotoxin-receptor complex in this system is 20 nM. The sea anemone toxin effect is antagonized by tetrodotoxin.Neurotoxins are essential tools for the analysis of molecular aspects of nerve conduction and transmission. Toxic molecules already available for study of molecular aspects of conduction include: (i) tetrodotoxin and saxitoxin, which are highly specific for blocking the Na+ channel in most axons (1, 2); (ii) veratridine and batrachotoxin, which depolarize nerve membrane by a selective increase in the resting sodium permeability (2-5); and (iii) scorpion neurotoxin, a miniprotein which affects reversibly the closing of the Na+ channel and the opening of the K+ channel (6-8).A series of neurotoxins was recently isolated in the pure form froln the sea anemone Anemonia sulcata (9-11). The toxins all are small polypeptides. MATERIALS AND METHODS Purification of sea anemone toxins (Anemonia sulcata) was carried out according to Beress et al. (9,10). ATX11 is the most abundant of the three neurotoxic polypeptides (9, 10, 12).Giant axons used in this work were those of the crayfish Astacus leptodactylus and of a cephalopod, the cuttlefish Sepia offlicnalis (axon diameter 200-400 Mum). Giant axons from crustacea were isolated from circumesophageal nerve connectives, those of Sepia from stellar nerves (13). Resting and action potential recordings and voltage clamp experiments have been previously described (8). When the nerve is bathed in a solution containing 0.1 nM ATX11 some of the thin axons begin to fire spontaneously (Fig. IA). More axons are affected at a concentration of 1 nM of ATX11.The giant axon having the maximum diameter (about 100 Mm), which has been used for microelectrode and voltage clamp analysis, is sensitive to ATX11 at concentrations higher than 0.1 AM (Fig. iC). Toxin action on this axon provokes a marked plateau phase of...

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“…Quinquestriatus toxin and toxin II greatly retarded the falling phase of the action potential of the rat diaphragm as previously reported for other nerve and muscles (Coraboeuf, Deroubaix & Tazieff-Depierre, 1975;Warnick et al, 1976;Bernard, Couraud & Lissitzky, 1977;Catterall, 1979;Alsen et al, 1981) and prolonged the 80% repolarization time 3 to 4 fold, whereas crotamine prolonged the time-course by only 30%. It has been concluded that scorpion and sea anemone toxins act mainly on the inactivation mechanism of the sodium channel (Koppenhofer & Schmidt, 1968;Bergman et al, 1976 (Figure 2) and that the number of binding sites for toxin II is in excess of that for scorpion toxin (Vincent, Balerna, Barhanin, Fosset & Lazdunski, 1980). Vincent et al (1980) reported that the binding of scorpion toxins to synaptosomes could be completely prevented by sea anemone toxin II, while the binding of the latter could not be prevented by scorpion toxins.…”

Section: Discussionmentioning

confidence: 99%

“…The third receptor site, located most probably on the external surface of the membrane, binds some polypeptide toxins isolated from scorpion venoms and sea anemone nematocysts. These group III toxins alter the inactivation process (Koppenhofer & Schmidt, 1968;Bergman, Dubois, Rojas & Rathmayer, 1976;Gillespie & Meves, 1980) and interact allosterically with group II toxins so that the persistent activation of the sodium channel is markedly enhanced (Catterall, 1977b;Catterall & Beress, 1978;Jacques, Fosset & Lazdunski, 1978;Tamkun & Catterall, 1981).…”

Section: Introductionmentioning

confidence: 99%

A study on the membrane depolarization of skeletal muscles caused by a scorpion toxin, sea anemone toxin II and crotamine and the interaction between toxins

Chang

Hong

1983

British J Pharmacology

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1 Quinquestriatus toxin (QTX) isolated from the venom of a scorpion (Leiurus quinquestriatus) and sea anemone (Anemonia sulcata) toxin II enhanced the twitch response of the rat and mouse diaphragms and like crotamine (isolated from the venom of Crotalus durissus terrificus) caused spontaneous fasciculation of the muscle. 2 Trains of action potentials in muscles at 70-250Hz, which could not be antagonized by (+)-tubocurarine, were triggered by single stimulation or occurred spontaneously after treatment with these toxins. 3 QTX and toxin II prolonged the rat muscle action potential 3 to 4 fold whereas crotamine prolonged the action potential by only 30%. 4 The membrane potential was depolarized from about -82mV to -55mV by crotamine 2 jigml -, -41 mV by toxin II 5 jig ml-and to -5OmV by QTX 1 jigml-1. The concentrations to induce 50% maximal depolarization (Ko.5) were 0.07, 0.15 and >0.4)jgml-1, respectively, for QTX, crotamine and toxin II, whereas the rates of depolarization were in the order toxin II > crotamine > QTX. The depolarizing effects of crotamine and QTX, but not of toxin II, were saturable.5 The depolarizing effects of all three toxins were irreversible whereas the membrane potential could be restored by tetrodotoxin non-competitively. 6 Simultaneous treatment with crotamine and QTX or crotamine and toxin II at concentrations below K0.5 caused only additive effects on depolarization. 7 When the muscle was depolarized by pretreating with a saturating concentration of crotamine, the onset of depolarization by QTX was greatly retarded whereas that by toxin II was unaffected. Action potentials were further prolonged in both cases.8 It is inferred that all three peptide toxins act at sites on the sodium channel and the binding sites for QTX and crotamine overlap to a considerable extent. On the other hand, the site for toxin II appears not to overlap with that of crotamine but may overlap with that of QTX.

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Die Wirkung von Skorpiongift auf die Ionenstr�me des Ranvierschen Schn�rrings

Cited by 129 publications

References 17 publications

Multiple kinetic components of sodium channel inactivation in rabbit Schwann cells.

Multiple kinetic components of sodium channel inactivation in rabbit Schwann cells.

Sea anemone toxin:a tool to study molecular mechanisms of nerve conduction and excitation-secretion coupling.

A study on the membrane depolarization of skeletal muscles caused by a scorpion toxin, sea anemone toxin II and crotamine and the interaction between toxins

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