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Results for “Scorpion toxin”

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At least 19 recordsLinked to original sources

PubMed1978

Sea anemone toxin and scorpion toxin share a common receptor site associated with the action potential sodium ionophore.

Toxin II isolated from the sea anemone Anemonia sulcata enhances activation of the action potential sodium ionophore of electrically excitable neuroblastoma cells by veratridine and batrachotoxin. This heterotropic cooperative effect is identical to that observed previously with scorpion toxin but occurs at a 110-fold higher concentration. Depolarization of the neuroblastoma cells inhibits the effect of sea anemone toxin as observed previously for scorpion toxin. Specific scorpion toxin binding is inhibited by sea anemone toxin with KD approximately equal to 90 nM. These results show that the polypeptides scorpion toxin and sea anemone toxin II share a common receptors site associated with action potential sodium ionophores.

Action Potentials↗

PubMed1979

Binding of scorpion toxin to receptor sites associated with sodium channels in frog muscle. Correlation of voltage-dependent binding with activation.

Purified scorpion toxin (Leiurus quinquestriatus) slows inactivation of sodium channels in frog muscle at concentrations in the range of 17-170 nM. Mono[125I]iodo scorpion toxin binds to a single class of sites in frog sartorius muscle with a dissociation constant of 14 nM and a binding capacity of 13 fmol/mg wet weight. Specific binding is inhibited more than 90% by 3 microM sea anemone toxin II and by depolarization with 165 mM K+. Half-maximal inhibition of binding is observed on depolarization to -41 mV. The voltage dependence of scorpion toxin binding is correlated with the voltage dependence of activation of sodium channels. Removal of calcium from the bathing medium shifts both activation and inhibition of scorpion toxin binding to more negative membrane potentials. The results are considered in terms of the hypothesis that activation of sodium channels causes a conformational change in the scorpion toxin receptor site resulting in reduced affinity for scorpion toxin.

Animals↗

PubMed1976

Membrane potential dependent binding of scorpion toxin to action potential Na+ ionophore.

Depolarization of neuroblastoma cells causes a 70-fold increase in the apparent dissociation constant KD for scorpion toxin enhancement of activation of the action potential Na+ ionophore by veratridine and a large increase in the rate of reversal of scorpion toxin action. Depolarization also inhibits binding of 125I-labeled scorpion toxin to a small number of saturable binding sites on electrically excitable neuroblastoma cells and increases the rate of dissociation of scorpion toxin from these sites. The results suggest that scorpion toxin binds to a regulatory component of the action potential Na+ ionophore whose conformation changes on depolarization.

Action Potentials↗

PubMed1976

Stimulation of glucagon secretion by scorpion toxin in the perfused rat pancreas.

Toxin from the scorpion Leiurus quinquestriatus was used to release norepinephrine from sympathetic nerve endings in the perfused rat pancrease. Addition of toxin, 10 mug./ml., to perfusate containing 0.3 mg./ml. glucose caused a large increase in release of norepinephrine and glucagon. Glucagon secretion was suppressed by perfusate containing 3.0 mg./ml. glucose but still responded to stimulation with scorpion toxin. Atropine, 10 muM, had no effect on either norepinephrine or glucagon release in response to scorpion toxin. The release of glucagon was blocked by 100 muM propranolol, 10 muM phentolamine, or 30 muM phenoxybenzamine. Somatostatin, 55nM, did not affect the release of norepinephrine by scorpion toxin but totally inhibited the glucagon response. These results suggest that pharmacologic stimulation of the adrenergic nerve endings in the rat pancreas can elicit a rapid release of glucagon. This response can be prevented by appropriate concentrations of either alpha or beta adrenergic blocking agents or somatostatin.

Animals↗

PubMed1975

Pharmacology of scorpion toxin II in the skeletal muscle.

1. Scorpion toxin II is potent in inducing contracture and spontaneous contractions of the chick biventer cervicis muscle. In addition, this toxin induces membrane depolarization and blockade of neuromuscular transmission in this muscle preparation. The purpose of the present study is to explore the possible mechanism of actions of toxin II. 2. The muscle contracture induced by toxin II is moderately accelerated by Ca2+-free Krebs solution, delayed by high Ca2+ (10 mM), high Mg2+ (10 mM) and low Na+ (60mM) Krebs solution. Moreover, this action is inhibited slightly by d-tubocurarine and completely by either procaine or tetrodotoxin, but unaffected by beta-bungarotoxin. All these findings suggest that toxin II induces contracture mainly by increasing the Na+ permeability of the muscle membrane. 3. Spontaneous contractions induced by toxin II are abolished by Ca2+-free Krebs solution, inhibited partially by either d-tubocurarine or beta-bungarotoxin and completely by tetrodotoxin or procaine. These results suggest that toxin II induces spontaneous contractions partially by releasing acetylcholine from nerve endings and partially by increasing the Na+ permeability of the muscle membrane.

Acetylcholine↗

PubMed1979

Electrophysiological studies on embryonic heart cells in culture. Scorpion toxin as a tool to reveal latent fast sodium channel.

Trypsin-dispersed heart cells were obtained from 11-day-old chick embryos. After culture as unstirred suspensions in dimethylsulfoxide-containing medium, spherical aggregates of cells beating spontaneously and apparently synchronously for months were obtained. Two kinds of cell were characterized by electrophysiological recordings: (1) cells with a slow rate of depolarizing phase showing tetrodotoxin-resistant action potential and blocked by D 600 ('slow' cells); (2) cells with high value of rising phase which was strongly decreased by tetrodotoxin and in which D 600 provoked uncoupling of excitation-contraction ('fast' cells). Toxin II from Androctonus australis scorpion venom increased the duration of action potential, which was ascribed to a slowing down of Na+ current inactivation and enhance the maximum rate of depolarization, especially in slow cells. Effects were antagonized by tetrodotoxin in both fast and slow cells. Washing experiments confirmed the results of previous studies, namely that tetrodotoxin and scorpion toxin bind to different receptors. It is concluded that slow cells with tetrodotoxin-resistant action potential contain latent fast Na+ channels that are revealed (activated) by toxin binding to the membrane.

Action Potentials↗

PubMed1976

Inhibition of insulin rlease by scorpion toxin in rat pancreatic islets.

Toxin purified from venom of the scorpion Leiurus quinquestriatus was used to release the norepinephrine from adrenergic nerve terminals in isolated pancreatic islets perifused in vitro. Addition of toxin (10 mug./ml) to the perifusion medium caused a sixfold increase in release of norepinephrine in the presence or absence of 3 X 10(-5) M phenoxybenzamine. During 20 minutes of stimulation with toxin, the pancreatic islets released an average of 15 pg. of norepinephrine per islet, which represented 20 per cent of the normal content of norepinephrine in islets. Insulin secretory rates in response to either 1.0 or 3.0 mg./ml. glucose were inhibited similarly by scorpion toxin. Addition of phenoxybenzamine abolished the inhibition of insulin release caused by scorpion toxin. Phenoxybenzamine alone did not affect release of insulin. Neither the enhanced release of norepinephrine nor the decreased release of insulin was reversed by a 20-minute wash-out period after infusion of toxin. These results indicate that the sympathetic nerve terminals in the rat pancreatic islet contain considerable amounts of norepinephrine that can be released by scorpion toxin. The norepinephrine released from sympathetic nerve endings in the pancreatic islet can inhibit release of insulin through an alpha-adrenergic action that is blocked by phenoxybenzamine.

Animals↗

PubMed1978

Mechanism of the pulmonary edema induced by intravenous injection of scorpion toxin in the rat.

The intravenous injection of purified scorpion toxin (tityustoxin, TsTX) into unanesthetized rats induces a severe systemic hypertension followed by a hemorrhagic edema of the lungs. The edema is focal or diffuse, whereas the hemorrhage is always focal and less prominent than the edema. Anesthesia of the rats prevents the appearance of pulmonary edema. It seems likely that this protective action of the anesthesia is due, at least in part, to an interference with the hypertension induced by TsTX. The pulmonary edema is prevented by bilateral adrenalectomy, guanethidine or phenoxybenzamine. It is suggested that the edema depends on a sympathetic-adrenal discharge and that catecholamines released by TsTX act on alpha adrenergic receptors. The mean kininogen content of the rat plasma, 1 h after TsTX injection, is not significantly different from that found in the control animals. The possible role played by kinins and other mediators in the early phases of the pulmonary edema induced by TsTX is under investigation.

Adrenalectomy↗

PubMed1978

Effect of scorpion toxin (tityustoxin, TsTx) on the salivary gland of the rat, in vivo and in vitro.

Intravenous injection of purified scorpion toxin (tityustoxin, TsTX) brings about the appearance of salivary flow and of kallikrein and amylase secretion in the saliva of rats. In experiments performed in vitro, using slices of parotid gland, a dose-response curve correlating tityustoxin concentration with kallikrein and amylase activities was obtained. The secretion of kallikrein is slower and smaller than that of amylase after up to 60 min of incubation. Experiments in which propranolol, phenoxybenzamine or atropine were injected into rats or added to parotid gland slices showed that the release of kallikrein is more dependent on cholinergic mechanisms, whereas the release of amylase is mainly related to adrenergic effects. Pre-treatment of the animals with reserpine confirms these results. The actions of tityustoxin on the kallikrein and amylase secretions, per min, are more effective than those by pilocarpine and isoproterenol, respectively.

Amylases↗

PubMed1977