AustralieFrV1, Main, Exploration, bibRecord, 009F11

Glycerotoxin stimulates neurotransmitter release from N-type Ca2+ channel expressing neurons

Identifieur interne : 009F11 ( Main/Exploration ); précédent : 009F10; suivant : 009F12

Glycerotoxin stimulates neurotransmitter release from N-type Ca2+ channel expressing neurons

Auteurs : Mitja Schenning [Australie] ; Dustin T. Proctor [Australie] ; Lotten Ragnarsson [Australie] ; Julien Barbier [France] ; Nickolas A. Lavidis [Australie] ; Jordi J. Molgo [France] ; Gerald W. Zamponi [Canada] ; Giampietro Schiavo [Royaume-Uni] ; Frederic A. Meunier [Australie, Royaume-Uni]

Source :

Journal of neurochemistry [ 0022-3042 ] ; 2006.

RBID : Pascal:06-0350536

Descripteurs français

Pascal (Inist)
- Neurotransmetteur, Libération, Neurone, Grenouille, Jonction neuromusculaire, Calcium, Préparation, Glutamate, Synaptosome, Sécrétion, Dépolarisation, Néonatal, Mammalia, Rat, Canal calcique N.
Wicri :
- topic : Calcium.

English descriptors

KwdEn :
- Calcium, Depolarization, Frog, Glutamate, Mammalia, N-type calcium channel, Neonatal, Neuromuscular junction, Neuron, Neurotransmitter, Preparation, Rat, Release, Secretion, Synaptosome.

Abstract

Glycerotoxin (GLTx) is capable of stimulating neurotransmitter release at the frog neuromuscular junction by directly interacting with N-type Ca²⁺ (Ca_v2.2) channels. Here we have utilized GLTx as a tool to investigate the functionality of Ca_v2.2 channels in various mammalian neuronal preparations. We first adapted a fluorescent-based high-throughput assay to monitor glutamate release from rat cortical synaptosomes. GLTx potently stimulates glutamate secretion and Ca²⁺ influx in synaptosomes with an EC₅₀ of 50 pM. Both these effects were prevented using selective Ca_v2.2 channel blockers suggesting the functional involvement of Ca_v2.2 channels in mediating glutamate release in this system. We further show that both Ca_v2. (P/Q-type) and Ca_v2.2 channels contribute equally to depolarization-induced glutamate release. We then investigated the functionality of Ca_v2.2 channels at the neonatal rat neuromuscular junction. GLTx enhances both spontaneous and evoked neurotransmitter release causing a significant increase in the frequency of postsynaptic action potentials. These effects were blocked by specific Ca_v2.2 channel blockers demonstrating that either GLTx or its derivatives could be used to selectively enhance the neurotransmitter release from Ca_v2.2-expressing mammalian neurons.

Affiliations:

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

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Le document en format XML

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<series><title level="j" type="main">Journal of neurochemistry</title>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Calcium</term>
<term>Depolarization</term>
<term>Frog</term>
<term>Glutamate</term>
<term>Mammalia</term>
<term>N-type calcium channel</term>
<term>Neonatal</term>
<term>Neuromuscular junction</term>
<term>Neuron</term>
<term>Neurotransmitter</term>
<term>Preparation</term>
<term>Rat</term>
<term>Release</term>
<term>Secretion</term>
<term>Synaptosome</term>
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<keywords scheme="Pascal" xml:lang="fr"><term>Neurotransmetteur</term>
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<term>Jonction neuromusculaire</term>
<term>Calcium</term>
<term>Préparation</term>
<term>Glutamate</term>
<term>Synaptosome</term>
<term>Sécrétion</term>
<term>Dépolarisation</term>
<term>Néonatal</term>
<term>Mammalia</term>
<term>Rat</term>
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<front><div type="abstract" xml:lang="en">Glycerotoxin (GLTx) is capable of stimulating neurotransmitter release at the frog neuromuscular junction by directly interacting with N-type Ca<sup>2+</sup>
 (Ca<sub>v</sub>
2.2) channels. Here we have utilized GLTx as a tool to investigate the functionality of Ca<sub>v</sub>
2.2 channels in various mammalian neuronal preparations. We first adapted a fluorescent-based high-throughput assay to monitor glutamate release from rat cortical synaptosomes. GLTx potently stimulates glutamate secretion and Ca<sup>2+</sup>
 influx in synaptosomes with an EC<sub>50</sub>
 of 50 pM. Both these effects were prevented using selective Ca<sub>v</sub>
2.2 channel blockers suggesting the functional involvement of Ca<sub>v</sub>
2.2 channels in mediating glutamate release in this system. We further show that both Ca<sub>v</sub>
2. (P/Q-type) and Ca<sub>v</sub>
2.2 channels contribute equally to depolarization-induced glutamate release. We then investigated the functionality of Ca<sub>v</sub>
2.2 channels at the neonatal rat neuromuscular junction. GLTx enhances both spontaneous and evoked neurotransmitter release causing a significant increase in the frequency of postsynaptic action potentials. These effects were blocked by specific Ca<sub>v</sub>
2.2 channel blockers demonstrating that either GLTx or its derivatives could be used to selectively enhance the neurotransmitter release from Ca<sub>v</sub>
2.2-expressing mammalian neurons.</div>
</front>
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Serveur d'exploration sur les relations entre la France et l'Australie

Glycerotoxin stimulates neurotransmitter release from N-type Ca2+ channel expressing neurons

Glycerotoxin stimulates neurotransmitter release from N-type Ca2+ channel expressing neurons

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