Effect of sea anemone toxins on the sodium inactivation process in crayfish axons.

Warashina, Akira; Fujita, Shozo

doi:10.1085/jgp.81.3.305

Cited by 53 publications

(28 citation statements)

References 34 publications

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“…The electrophysiological effects of ATX-II and ␣-scorpion toxins on macroscopic TTX-S sodium currents include the inhibition of the Na ϩ channel inactivation (Pelhate et al, 1984;Neumcke et al, 1985), the presence of sodium currents after prolonged depolarization (Warashina and Fujita, 1983), and voltage-dependent action (Strichartz and Wang, 1986). The effects of both BgII and BgIII are very similar.…”

Section: Discussionmentioning

confidence: 99%

The Sea Anemone Toxins BgII and BgIII Prolong the Inactivation Time Course of the Tetrodotoxin-Sensitive Sodium Current in Rat Dorsal Root Ganglion Neurons

Salceda¹,

Garateix²,

Soto³

2002

J Pharmacol Exp Ther

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We have characterized the effects of BgII and BgIII, two sea anemone peptides with almost identical sequences (they only differ by a single amino acid), on neuronal sodium currents using the whole-cell patch-clamp technique. Neurons of dorsal root ganglia of Wistar rats (P5-9) in primary culture (LeibovitzЈs L15 medium; 37°C, 95% air/5% CO 2 ) were used for this study (n ϭ 154). These cells express two sodium current subtypes: tetrodotoxin-sensitive (TTX-S; K i ϭ 0.3 nM) and tetrodotoxinresistant (TTX-R; K i ϭ 100 M). Neither BgII nor BgIII had significant effects on TTX-R sodium current. Both BgII and BgIII produced a concentration-dependent slowing of the TTX-S sodium current inactivation (IC 50 ϭ 4.1 Ϯ 1.2 and 11.9 Ϯ 1.4 M, respectively), with no significant effects on activation time course or current peak amplitude. For comparison, the concentration-dependent action of Anemonia sulcata toxin II (ATX-II), a well characterized anemone toxin, on the TTX-S current was also studied. ATX-II also produced a slowing of the TTX-S sodium current inactivation, with an IC 50 value of 9.6 Ϯ 1.2 M indicating that BgII was 2.3 times more potent than ATX-II and 2.9 times more potent than BgIII in decreasing the inactivation time constant ( h ) of the sodium current in dorsal root ganglion neurons. The action of BgIII was voltage-dependent, with significant effects at voltages below Ϫ10 mV. Our results suggest that BgII and BgIII affect voltage-gated sodium channels in a similar fashion to other sea anemone toxins and ␣-scorpion toxins.

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Section: Discussionmentioning

confidence: 99%

The Sea Anemone Toxins BgII and BgIII Prolong the Inactivation Time Course of the Tetrodotoxin-Sensitive Sodium Current in Rat Dorsal Root Ganglion Neurons

Salceda¹,

Garateix²,

Soto³

2002

J Pharmacol Exp Ther

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“…Recently, Warashina and Fujita (1983) reported that in crayfish axons, the time course of Na channel inactivation, which was adequately fitted with one single exponential, was clearly slowed by a purified sea anemone toxin. They also observed that less inactivation occurred at the more positive potentials, a finding qualitatively comparable to this report, and they postulated, similarly, that inactivated Na channels can reopen at more positive potentials.…”

Section: Kinetic Modelsfor Toxin-modified Na Channelsmentioning

confidence: 99%

Kinetic analysis of the action of Leiurus scorpion alpha-toxin on ionic currents in myelinated nerve.

Wang¹,

Strichartz²

1985

The Journal of General Physiology

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A BS T R A C T The effects of a neurotoxin, purified from the venom of the scorpion Leiurus quinquestriatus, on the ionic currents of toad single myelinated fibers were studied under voltage-clamp conditions. Unlike previous investigations using crude scorpion venom, purified Leiurus toxin IIa at high concentrations (200-400 nM) did not affect the K currents, nor did it reduce the peak Na current in the early stages of treatment. The activation of the Na channel was unaffected by the toxin, the activation time course remained unchanged, and the peak Na current vs. voltage relationship was not altered. In contrast, Na channel inactivation was considerably slowed and became incomplete . As a result, a steady state Na current was maintained during prolonged depolarizations of several seconds. These steady state Na currents had a different voltage dependence from peak Na currents and appeared to result from the opening of previously inactivated Na channels . The opening kinetics of the steady state current were exponential and had rates -100-fold slower than the normal activation processes described for transitions from the resting state to the open state. In addition, the dependence of the peak Na current on the potential of preceding conditioning pulses was also dramatically altered by toxin treatment; this parameter reached a minimal value near a membrane potential of -50 mV and then increased continuously to a "plateau" value at potentials greater than +50 mV. The amplitude of this plateau was dependent on toxin concentration, reaching a maximum value equal to -50% of the peak current; voltagedependent reversal of the toxin's action limits the amplitude of the plateauing effect . The measured plateau effect was half-maximum at a toxin concentration of 12 nM, a value quite similar to the concentration producing half of the maximum slowing of Na channel inactivation . The results of Hill plots for these actions suggest that one toxin molecule binds to one Na channel. Thus, the binding of a single toxin molecule probably both produces the steady state currents and slows the Na channel inactivation . We propose that Leiurus toxin inhibits the conversion of the open state to inactivated states in a voltagedependent manner, and thereby permits a fraction of the total Na permeability to remain at membrane potentials where inactivation is normally complete .

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“…This second possibility is, in some ways, more attractive, since it is consistent with the view that the primary action of ATX-II is to delay the inactivation of fast Na' channels (Neumcke et al, 1980;Ulbricht & Schmidtmayer, 1981;Warashina & Fujita, 1983).…”

Section: Discussionmentioning

confidence: 52%

The effects of Anemonia sulcata toxin II on vertebrate skeletal muscle

Harris

Pollard

Tesseraux

1985

British J Pharmacology

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Hospital, Westgate Road, Newcastle upon Tyne, NE4 6BE 1 Some effects of the sea anemone toxin, ATX-II, on vertebrate skeletal muscle have been described.2 At a concentration of 1 x IO-'-1 x 10-6M, ATX-I1 caused a sodium-dependent depolarizaton of the muscle fibres of the rat soleus and extensor digitorum longus, of the mouse soleus and extensor digitorum longus and of the chicken posterior latissimus dorsi. The muscle fibres of the frog sartorius were insensitive to the toxin. 3 Action potentials generated by direct stimulation were prolonged by ATX-II, but the degree of prolongation was variable. Chicken posterior latissimus dorsi muscle fibres were most sensitive in this regard, and mouse extensor digitorum longus were least sensitive. 4 Both denervated and immature muscle fibres were more sensitive to ATX-II than mature innervated muscle fibres. The sensitivity to ATX-II declined rapidly as muscle fibres matured. 5 In some muscles, the prolongation of the action potential was enhanced by repetitive stimulation, but not by the passive depolarization or hyperpolarization of the muscle fibres. 6 The actions of ATX-II could be reversed by washing in all but the innervated soleus of the mature rat.

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Effect of sea anemone toxins on the sodium inactivation process in crayfish axons.

Cited by 53 publications

References 34 publications

The Sea Anemone Toxins BgII and BgIII Prolong the Inactivation Time Course of the Tetrodotoxin-Sensitive Sodium Current in Rat Dorsal Root Ganglion Neurons

The Sea Anemone Toxins BgII and BgIII Prolong the Inactivation Time Course of the Tetrodotoxin-Sensitive Sodium Current in Rat Dorsal Root Ganglion Neurons

Kinetic analysis of the action of Leiurus scorpion alpha-toxin on ionic currents in myelinated nerve.

The effects of Anemonia sulcata toxin II on vertebrate skeletal muscle

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