Ouabain-induced increase in dopamine release from mouse striatal slices is antagonized by riluzole
Identifieur interne : 004143 ( Main/Exploration ); précédent : 004142; suivant : 004144Ouabain-induced increase in dopamine release from mouse striatal slices is antagonized by riluzole
Auteurs : A. Boireau [France] ; M. Meunier [France] ; A. Imperato [France]Source :
- Journal of pharmacy and pharmacology [ 0022-3573 ] ; 1998.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Calcium.
English descriptors
- KwdEn :
Abstract
We have examined the effects of riluzole, a neuroprotective drug which stabilizes voltage-dependent sodium channels in their inactivated state and inhibits the release of glutamate in-vivo and in-vitro, on the release of newly taken up [3H]dopamine induced by ouabain, a potent and selective inhibitor of Na+/K+-ATPase in mouse striatal slices in-vitro. Riluzole potently (IC50 (concentration resulting in 50% inhibition)=0.9±0.3 μM) and dose-dependently antagonized ouabain-stimulated [3H]dopamine release, the effect being observed at low concentrations. Tetrodotoxin (1 μM) and nomifensine (10 μM) also abolished ouabain-induced [3H]dopamine release. Blockade of glutamate receptors with dizocilpine (1 μM) and 6-(1H-imidazol-1-yl)-7-nitro-2,3(1H,4H)-quinoxalinedione (YM-90K; 10 μM), alone or in combination, was without effect. Incubation of striatal slices with 50 μM La3+, which blocks voltage-dependent calcium channels, did not inhibit [3H]dopamine release induced by ouabain. The potent effects of riluzole observed in this model are probably related to its ability to block voltage-dependent sodium channels. The consequences of this activity are critically discussed in relation to the protective action of riluzole previously reported in various models of Parkinson's disease and other neurodegenerative disorders.
Affiliations:
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Le document en format XML
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<term>Benzothiazole</term>
<term>Biological activity</term>
<term>Calcium</term>
<term>Calcium antagonist</term>
<term>Catecholamine</term>
<term>Central nervous system</term>
<term>Corpus striatum</term>
<term>Dopamine</term>
<term>In vitro</term>
<term>Ionic channel</term>
<term>Mechanism of action</term>
<term>Mouse</term>
<term>Neuroprotective agent</term>
<term>Neurotransmitter</term>
<term>Psychotropic</term>
<term>Riluzole</term>
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<keywords scheme="Pascal" xml:lang="fr"><term>Riluzole</term>
<term>Anticonvulsivant</term>
<term>Psychotrope</term>
<term>Activité biologique</term>
<term>Mécanisme action</term>
<term>Animal</term>
<term>Souris</term>
<term>Système nerveux central</term>
<term>Corps strié</term>
<term>In vitro</term>
<term>Dopamine</term>
<term>Catécholamine</term>
<term>Neurotransmetteur</term>
<term>Antagoniste calcium</term>
<term>Neuroprotecteur</term>
<term>Canal ionique</term>
<term>Calcium</term>
<term>Benzothiazole</term>
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<front><div type="abstract" xml:lang="en">We have examined the effects of riluzole, a neuroprotective drug which stabilizes voltage-dependent sodium channels in their inactivated state and inhibits the release of glutamate in-vivo and in-vitro, on the release of newly taken up [<sup>3</sup>
H]dopamine induced by ouabain, a potent and selective inhibitor of Na<sup>+</sup>
/K<sup>+</sup>
-ATPase in mouse striatal slices in-vitro. Riluzole potently (IC50 (concentration resulting in 50% inhibition)=0.9±0.3 μM) and dose-dependently antagonized ouabain-stimulated [<sup>3</sup>
H]dopamine release, the effect being observed at low concentrations. Tetrodotoxin (1 μM) and nomifensine (10 μM) also abolished ouabain-induced [<sup>3</sup>
H]dopamine release. Blockade of glutamate receptors with dizocilpine (1 μM) and 6-(1H-imidazol-1-yl)-7-nitro-2,3(1H,4H)-quinoxalinedione (YM-90K; 10 μM), alone or in combination, was without effect. Incubation of striatal slices with 50 μM La<sup>3+</sup>
, which blocks voltage-dependent calcium channels, did not inhibit [<sup>3</sup>
H]dopamine release induced by ouabain. The potent effects of riluzole observed in this model are probably related to its ability to block voltage-dependent sodium channels. The consequences of this activity are critically discussed in relation to the protective action of riluzole previously reported in various models of Parkinson's disease and other neurodegenerative disorders.</div>
</front>
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