AustralieFrV1, Main, Exploration, bibRecord, 007A48

Analysis of Caribbean ciguatoxin-1 effects on frog myelinated axons and the neuromuscular junction

Identifieur interne : 007A48 ( Main/Exploration ); précédent : 007A47; suivant : 007A49

Analysis of Caribbean ciguatoxin-1 effects on frog myelinated axons and the neuromuscular junction

Auteurs : César Mattei [France] ; Michel Marquais [France] ; Sébastien Schlumberger [France] ; Jordi Molgo [France] ; Jean-Paul Vernoux [France] ; Richard J. Lewis [Australie] ; Evelyne Benoit [France]

Source :

Toxicon : (Oxford) [ 0041-0101 ] ; 2010.

RBID : Pascal:10-0467262

Descripteurs français

Pascal (Inist)
- Acétylcholine, Mer des Caraïbes, Ciguatoxine, Amphibia, Grenouille, Animal, Axone, Jonction neuromusculaire, Electrophysiologie, Microscopie confocale, Potentiel membrane, Libération, Ion sodium, Sodium, Canal ionique.
Wicri :
- topic : Sodium.

English descriptors

KwdEn :
- Acetylcholine, Amphibia, Animal, Axon, Caribbean Sea, Confocal microscopy, Electrophysiology, Frog, Ionic channel, Membrane potential, Neuromuscular junction, Release, Sodium, Sodium ion.

Abstract

Caribbean ciguatoxin-1 (C-CTX-1) induced, after about 1 h exposure, muscle membrane depolarisation and repetitive post-synaptic action potentials (APs) in frog neuromuscular preparations. This depolarising effect was also observed in a Ca²⁺-free medium with a strong enhancement of spontaneous quantal transmitter release, compared with control conditions. The ciguatoxin-induced increase in release could be accelerated when Ca²⁺ was present in the extracellular medium. C-CTX-1 also enhanced nerve-evoked quantal acetylcholine (ACh) release. At normal neuromuscular junctions loaded with the fluorescent dye FM1-43, C-CTX-1 induced swelling of nerve terminals, an effect that was reversed by hyperosmotic D-mannitol. In myelinated axons, C-CTX-1 increased nodal membrane excitability, inducing spontaneous and repetitive APs. Also, the toxin enlarged the repolarising phase of APs in control and tetraethylammonium-treated axons. Overall, our data suggest that C-CTX-1 affects nerve excitability and neurotransmitter release at nerve terminals. We conclude that C-CTX-1-induced up-regulation of Na⁺ channels and the inhibition of K⁺ channels, at low nanomolar concentrations, produce a variety of functional dysfunctions that are in part responsible for the human muscle skeletal symptoms observed in ciguatera. All these dysfunctions seem to result from the subtle balance between ionic currents, intracellular Na⁺ and Ca²⁺ concentrations, and engaged second messengers.

Affiliations:

Australie, France

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Le document en format XML

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<series><title level="j" type="main">Toxicon : (Oxford)</title>
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<term>Animal</term>
<term>Axon</term>
<term>Caribbean Sea</term>
<term>Confocal microscopy</term>
<term>Electrophysiology</term>
<term>Frog</term>
<term>Ionic channel</term>
<term>Membrane potential</term>
<term>Neuromuscular junction</term>
<term>Release</term>
<term>Sodium</term>
<term>Sodium ion</term>
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<keywords scheme="Pascal" xml:lang="fr"><term>Acétylcholine</term>
<term>Mer des Caraïbes</term>
<term>Ciguatoxine</term>
<term>Amphibia</term>
<term>Grenouille</term>
<term>Animal</term>
<term>Axone</term>
<term>Jonction neuromusculaire</term>
<term>Electrophysiologie</term>
<term>Microscopie confocale</term>
<term>Potentiel membrane</term>
<term>Libération</term>
<term>Ion sodium</term>
<term>Sodium</term>
<term>Canal ionique</term>
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<front><div type="abstract" xml:lang="en">Caribbean ciguatoxin-1 (C-CTX-1) induced, after about 1 h exposure, muscle membrane depolarisation and repetitive post-synaptic action potentials (APs) in frog neuromuscular preparations. This depolarising effect was also observed in a Ca<sup>2+</sup>
-free medium with a strong enhancement of spontaneous quantal transmitter release, compared with control conditions. The ciguatoxin-induced increase in release could be accelerated when Ca<sup>2+</sup>
 was present in the extracellular medium. C-CTX-1 also enhanced nerve-evoked quantal acetylcholine (ACh) release. At normal neuromuscular junctions loaded with the fluorescent dye FM1-43, C-CTX-1 induced swelling of nerve terminals, an effect that was reversed by hyperosmotic D-mannitol. In myelinated axons, C-CTX-1 increased nodal membrane excitability, inducing spontaneous and repetitive APs. Also, the toxin enlarged the repolarising phase of APs in control and tetraethylammonium-treated axons. Overall, our data suggest that C-CTX-1 affects nerve excitability and neurotransmitter release at nerve terminals. We conclude that C-CTX-1-induced up-regulation of Na<sup>+</sup>
 channels and the inhibition of K<sup>+</sup>
 channels, at low nanomolar concentrations, produce a variety of functional dysfunctions that are in part responsible for the human muscle skeletal symptoms observed in ciguatera. All these dysfunctions seem to result from the subtle balance between ionic currents, intracellular Na<sup>+</sup>
 and Ca<sup>2+</sup>
 concentrations, and engaged second messengers.</div>
</front>
</TEI>
<affiliations><list><country><li>Australie</li>
<li>France</li>
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<tree><country name="France"><noRegion><name sortKey="Mattei, Cesar" sort="Mattei, Cesar" uniqKey="Mattei C" first="César" last="Mattei">César Mattei</name>
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<name sortKey="Vernoux, Jean Paul" sort="Vernoux, Jean Paul" uniqKey="Vernoux J" first="Jean-Paul" last="Vernoux">Jean-Paul Vernoux</name>
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<country name="Australie"><noRegion><name sortKey="Lewis, Richard J" sort="Lewis, Richard J" uniqKey="Lewis R" first="Richard J." last="Lewis">Richard J. Lewis</name>
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Analysis of Caribbean ciguatoxin-1 effects on frog myelinated axons and the neuromuscular junction

Analysis of Caribbean ciguatoxin-1 effects on frog myelinated axons and the neuromuscular junction

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Descripteurs français

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

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