Characterization of the palytoxin‐induced sodium conductance in frog skeletal muscle

Ecault, E.; Sauviat, Martin-Pierre

doi:10.1111/j.1476-5381.1991.tb12204.x

Cited by 23 publications

(8 citation statements)

References 28 publications

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“…This effect excludes Ca 2+ entry through PTX channels being responsible for the effect of the toxin on [Ca 2+ ] c (Monroe and Tashjian,1995). PTX‐induced depolarization has been shown to be only partially sensitive to tetrodotoxin in most cell types but dependent on extracellular Na + concentration (Kudo and Shibata,1980; Castle and Strichartz,1988; Ecault and Sauviat,1991).…”

Section: Discussionmentioning

confidence: 99%

Modulation of calcium entry and glutamate release in cultured cerebellar granule cells by palytoxin

Vale¹,

Alfonso²,

Suñol

et al. 2006

J of Neuroscience Research

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A channel open on the membrane can be formed by palytoxin (PTX). Ten nanomolar PTX caused an irreversible increase in the cytosolic calcium concentration ([Ca(2+)](c)), which was abolished in the absence of external calcium. The increase was eliminated by saxitoxin (STX) and nifedipine (NIF). Calcium rise is secondary to the membrane depolarization. PTX effect on calcium was dependent on extracellular Na(+). Li(+) decreased the PTX-evoked rise in [Ca(2+)](c); replacement of Na(+) by N-methyl-D-glucamine (NMDG) abolished PTX-induced calcium increase. [Ca(2+)](c) increase by PTX was strongly reduced after inhibition of the reverse operation of the Na(+)/Ca(2+) exchanger, in the presence of antagonists of excitatory amino acid (EAA) receptors, and by inhibition of neurotransmitter release. PTX did not modify calcium extrusion by the plasma membrane Ca(2+)-ATPase (PMCA), because blockade of the calcium pump increased rather than decreased the PTX-induced calcium influx. Extracellular levels of glutamate and aspartate were measured by HPLC and exocytotic neurotransmitter release by determination of synaptic vesicle exocytosis using total internal reflection fluorescence microscopy (TIRFM). PTX caused a concentration-dependent increase in EAA release to the culture medium. Ten nanomolar PTX decreased cell viability by 30% within 5 min. PTX-induced calcium influx involves three pathways: Na(+)-dependent activation of voltage-dependent sodium channels (VDSC) and voltage-dependent calcium channels (VDCC), reverse operation of the Na(+)/Ca(2+) exchanger, and indirect activation of EAA receptors through glutamate release. The neuronal injury produced by the toxin could be partially mediated by the PTX-induced overactivation of EAA receptors, VDSC, VDCC and the glutamate efflux into the extracellular space.

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Section: Discussionmentioning

confidence: 99%

Modulation of calcium entry and glutamate release in cultured cerebellar granule cells by palytoxin

Vale¹,

Alfonso²,

Suñol

et al. 2006

J of Neuroscience Research

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“…The activity of PLTX has been investigated in various different excitable cell models. In these models, PLTX causes a depolarization of the cellular membrane, − which affects the mechanisms controlling intracellular calcium concentration ([Ca 2+ ] i ). The documented biological effects triggered by PLTX-induced depolarization include the disruption of the excitation–contraction coupling in cardiac cells, contraction of smooth muscles, − and the release of neurotransmitters …”

Section: Introductionmentioning

confidence: 99%

The Stretch-Activated Channel Blocker Gd³⁺Reduces Palytoxin Toxicity in Primary Cultures of Skeletal Muscle Cells

Favero¹,

Florio²,

Codan³

et al. 2012

Chem. Res. Toxicol.

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Palytoxin (PLTX) is one of the most toxic seafood contaminants ever isolated. Reports of human food-borne poisoning ascribed to PLTX suggest skeletal muscle as a primary target site. Primary cultures of mouse skeletal muscle cells were used to study the relationship between Ca(2+) response triggered by PLTX and the development of myotoxic insult. Ca(2+) imaging experiments revealed that PLTX causes a transitory intracellular Ca(2+) response (transient phase) followed by a slower and more sustained Ca(2+) increase (long-lasting phase). The transient phase is due to Ca(2+) release from intracellular stores and entry through voltage-dependent channels and the Na(+)/Ca(2+) exchanger (reverse mode). The long-lasting phase is due to a massive and prolonged Ca(2+) influx from the extracellular compartment. Sulforhodamine B assay revealed that the long-lasting phase is the one responsible for the toxicity in skeletal muscle cells. Our data analyzed, for the first time, pathways of PLTX-induced Ca(2+) entry and their correlation with PLTX-induced toxicity in skeletal muscle cells. The cellular morphology changes induced by PLTX and the sensitivity to gadolinium suggest a role for stretch-activated channels.

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“…The remaining PTX-activated 22Na' flux is blocked by 3,4 dichlorobenzamil, another derivative of amiloride that is well known to block the Na+/Ca2+ exchange activity (Frelin et al, 1990a). Finally, amiloride has been reported to block PTX-induced inward currents in frog skeletal muscles (Ecault & Sauviat, 1991). In this study, we characterize PTX-induced channels in aortic myocytes with a combination of 22Na' uptake measurements and single channel current recordings, and define the properties of interaction of this channel with amiloride derivatives and with ouabain.…”

Section: Introductionmentioning

confidence: 99%

3,4 Dichlorobenzamil‐sensitive, monovalent cation channel induced by palytoxin in cultured aortic myocytes

Renterghem

Frelin

1993

British J Pharmacology

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1 Smooth muscle cells were dispersed from rat aorta and then cultured. The action of palytoxin on rat aortic myocytes was analysed by measurement of 22Na+ uptake and single channel recording techniques. 2 Palytoxin induced an increase in 22Na+ uptake, with a concentration of 50 nM producing halfmaximal activation. The action of palytoxin was inhibited by amiloride derivatives and by ouabain. The concentrations of inhibitor producing half-maximal inhibition were 10 JIM for 3,4 dichlorobenzamil, 30 JAM for benzamil, 100 JAM for phenamil and 1 mm for ouabain. 3 In outside-out patches, palytoxin induced single channel currents that reversed near 0 mV with NaCl or KCI in the extracellular solution, but were outward with N-methyl-D-glucamine chloride or CaCl2 ( 10 mM), indicating that palytoxin induced a cation channel permeable to Na+ and K+ (PK/PNa = 1.2) but not to Ca2+ (PK/PCa > 30) or to N-methyl-D-glucamine (NMDG) (PK/PNMDG> 11). The unit channel conductance was 11 -14 pS. 4 A high (>0.1 mM) extracellular concentration of Ca2+ was necessary to observe channel activation by palytoxin. A high (150 mM) extracellular concentration of K+ partially prevented and reversed channel activation by palytoxin. 5 The channel activity was fully blocked by 3,4 dichlorobenzamil (20 JAM) and partially blocked by phenamil (50 JM). It was not reduced by ouabain (200 JAM).

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Characterization of the palytoxin‐induced sodium conductance in frog skeletal muscle

Cited by 23 publications

References 28 publications

Modulation of calcium entry and glutamate release in cultured cerebellar granule cells by palytoxin

Modulation of calcium entry and glutamate release in cultured cerebellar granule cells by palytoxin

The Stretch-Activated Channel Blocker Gd³⁺Reduces Palytoxin Toxicity in Primary Cultures of Skeletal Muscle Cells

3,4 Dichlorobenzamil‐sensitive, monovalent cation channel induced by palytoxin in cultured aortic myocytes

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Characterization of the palytoxin‐induced sodium conductance in frog skeletal muscle

Cited by 23 publications

References 28 publications

Modulation of calcium entry and glutamate release in cultured cerebellar granule cells by palytoxin

Modulation of calcium entry and glutamate release in cultured cerebellar granule cells by palytoxin

The Stretch-Activated Channel Blocker Gd3+Reduces Palytoxin Toxicity in Primary Cultures of Skeletal Muscle Cells

3,4 Dichlorobenzamil‐sensitive, monovalent cation channel induced by palytoxin in cultured aortic myocytes

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The Stretch-Activated Channel Blocker Gd³⁺Reduces Palytoxin Toxicity in Primary Cultures of Skeletal Muscle Cells