Block of locust muscle glutamate receptors by δ-philathotoxin occurs after receptor activations

Clark, R.B.; Donaldson, P. Lynn; Gration, K.A.F.; Lambert, Jeremy J.; Piek, T.; Ramsey, R. L.; Spanjer, W.; Usherwood, P.N.R.

doi:10.1016/0006-8993(82)91233-1

Cited by 81 publications

(27 citation statements)

References 17 publications

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“…The clear reversibility of the toxin effects after washing could also be explained by a lower toxin-receptor affinity. Conceptually similar models, whereby toxin binding induces a change in receptor conformation or function, consequently lowering the toxin-receptor affinity, have been suggested for a-toxins from scorpion venoms (Catterall, 1986) and polyamine toxins from digger wasp venoms (Clark et al, 1982). It is noteworthy that the reversibility of C. textile toxin effects after washing strongly contrasts the irreversibility of w-conotoxins, which bind to mammalian neuronal preparations at Kd values in the picomolar range (Gray et al, 1988).…”

Section: Electrophysiologymentioning

confidence: 94%

Mollusc‐specific toxins from the venom of Conus textile neovicarius

Fainzilber

Gordon

Hasson

et al. 1991

European Journal of Biochemistry

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Three peptide toxins exhibiting strong paralytic activity to molluscs, but with no paralytic effects on arthropods or vertebrates, were purified from the venom of the molluscivorous snail Conus textile neovicarius from the Red Sea. The amino acid sequences of these mollusc specific toxins are: TxIA, WCKQSGEMCNLLDQNCCDGYCIVLVCT (identical to the so called ‘King Kong peptide’); TxIB, WCKQSGEMCNVLDQNCCDGYCIVFVCT; TxIIA, WGGYSTYCγVDSγCCSDNCVRSYCT (γ=γ‐carboxyglutamate). There is a similarity of the Cys framework of these toxins to that of the ω‐conotoxins; however, their net negative charges, high content of hydrophobic residues and uneven number of Cys residues in TxIIA, are highly unusual for conotoxins. When assayed on isolated cultured Aplysia neurons, all three toxins induced membrane depolarization and spontaneous repetitive firing. The TxI toxins also induce a marked prolongation of the action potential duration, which is sodium dependent. These effects differ significantly from the blocking activities of piscivorous venom conotoxins. These mollusc specific conotoxins may therefore serve as new and selective probes for ion‐channel functions in molluscan neuronal systems.

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Section: Electrophysiologymentioning

confidence: 94%

Mollusc‐specific toxins from the venom of Conus textile neovicarius

Fainzilber

Gordon

Hasson

et al. 1991

European Journal of Biochemistry

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“…In the present study, TI-233 depressed the glutamateinduced responses in a stimulus frequency-dependent manner, whereas it had no marked effect on the unit size of ej.ps evoked at low frequencies, but ej.ps continuously evoked at high frequencies gradually declined under the influence of the drug. In some respects, the mode of action of TI-233 on the glutamate response seems to resemble that of6-philanthotoxin (Clark et al, 1982) or that of SKF-525A on the acetylcholine response (Magazanik et al, 1982). Chlorisondamine and trimethaphan are powerful glutamate inhibitors of similar potency to TI-233, but they depressed both glutamate responses and e j.ps in a similar manner (Lingle et al, 1981;Shinozaki et al, 1982;Shinozaki & Ishida, 1983a,b).…”

Section: Discussionmentioning

confidence: 99%

“…While the agonist is present, receptors might be gradually converted into the 'channel blocked' state resulting from preceding channel openings. If the unblocking rate constant which limits the speed of recovery is extremely small, the number of free receptors available would eventually become very small (Clark et al, 1982). The unit size for continuously evoked ej.ps should be gradually reduced when the muscle fibre is immersed in the TI-233 solution for a prolonged period, because, unlike chlorisondamine, the unblocking rate constant of TI-233 is presumed to be very small.…”

Section: Discussionmentioning

confidence: 99%

TI‐233 as a glutamate channel blocker at the crayfish neuromuscular junction

Ishida

Shinozaki

1985

British J Pharmacology

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1 Effects of TI-233 (4-isopropyl-l-[N2-(5,6-dimethyl-aminonaphthalene-I -sulphonyl)-L-arginyl]-piperidine) on glutamate-induced responses and nerve-evoked synaptic responses were compared at the crayfish neuromuscular junction. 2 Intracellularly recorded excitatory junctional potentials (ej.ps) were markedly augmented by TI-233 when they were evoked at long intervals, whereas the unit size of extracellular ej.ps was hardly affected by at that stage, the glutamate-induced current was markedly reduced by The decay rate of extracellular ej.ps was slightly increased 3 min after the addition of TI-233 at concentrations higher than 0.05 mM. 4 Repetitive stimulation of the excitatory axon at a high frequency caused a gradual decrease in the amplitudes of extracellular e j.ps in the presence ofTI-233. After prolonged application of TI-233 with repetitive nerve stimulation, the glutamate-induced response became significantly smaller than the control. 5 TI-233 increased the input resistance of the crayfish muscle fibre and facilitated transmitter release at the excitatory neuromuscular junction. These two effects would entirely explain the augmentation of intracellular ej.ps by TI-233.6 TI-233 (> 3 gM) reduced the amplitude ofcurrent responses to trains of glutamate pulses in a dosedependent manner, but this reduction by TI-233 was time-and activity-dependent. The effect ofTI-233 on glutamate-induced responses was voltage-dependent and hyperpolarization increased this effect. 7 Pretreatment of the muscle fibre with concanavalin A did not affect the gradual decline, caused by TI-233, of the successive currents evoked by a train of glutamate pulses. 8 The apparent differences between the glutamate-induced current and nerve-evoked synaptic response revealed by TI-233 can be explained by open-channel block of the glutamate-activated ionchannel, and do not confute the hypothesis that glutamate is the natural transmitter substance at this junction. IntroductionGlutamate is a putative excitatory transmitter at the crayfish neuromuscular junction, and several criteria for transmitter identification other than the pharmacological criterion have been satisfactorily met at this site (Takeuchi & Takeuchi, 1964;Onodera & Takeuchi, 1975;1976;1980;Kawagoe et al., 1981;1982). Glutamate exists in sufficient quantities in the presynaptic terminals, and stimulation of the excitatory axons causes a release of glutamate in adequate quantities from the presynaptic terminals (Kawagoe et al., 1981;1982 (Shinozaki, 1980). So far, at the crayfish neuromuscular junction, there appear to be some differences between the action of some agents on the nerve-evoked junctional response and their effect on the glutamate response (Shinozaki & Ishida, 1979a, b;Ishida & Shinozaki, 1980;Shinozaki, 1980). Diltiazem and its structural analogue, caroverine, which are potent Ca antagonists, depressed the responses of the crayfish muscle to glutamate without affecting the average unit size of extracellular ej.ps (Ishida & Shinozaki, 1980;. In addition to these ...

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“…Wasp toxins also are sources of metabolites with affinity for iGluRs. Philanthotoxins, which are polyamine-containing toxins from the digger wasp Philanthus triangulum, and Joro spider toxins (JSTX) from the Joro spider Nephila clavata are open-channel blockers for a subset of glutamate receptors (Clark et al 1982;Bruce et al 1990;Blagbrough et al 1994;Usherwood 2000;Estrada et al 2007). Numerous other examples of molecules derived from terrestrial organisms exist whose activity on iGluRs have been characterized to varying degrees (e.g., Takemoto et al 1964;Evans and Usherwood 1985;Konno et al 1988;Shin-ya et al 1997a, b;McCormick et al 1999;Watanabe and Kitahara 2007).…”

Section: Fig 1 Chemical Structures Of Representative Iglur Ligands Dmentioning

confidence: 99%

Developmental Biology of Neoplastic Growth

Macieira‐Coelho¹

2005

Progress in Molecular and Subcellular Biology

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Block of locust muscle glutamate receptors by δ-philathotoxin occurs after receptor activations

Cited by 81 publications

References 17 publications

Mollusc‐specific toxins from the venom of Conus textile neovicarius

Mollusc‐specific toxins from the venom of Conus textile neovicarius

TI‐233 as a glutamate channel blocker at the crayfish neuromuscular junction

Developmental Biology of Neoplastic Growth

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