Riluzole reduces hyperactivity of subthalamic neurons induced by unilateral 6-OHDA lesion in the rat brain.
Identifieur interne : 001227 ( PubMed/Corpus ); précédent : 001226; suivant : 001228Riluzole reduces hyperactivity of subthalamic neurons induced by unilateral 6-OHDA lesion in the rat brain.
Auteurs : O K Hassani ; M. Mouroux ; G A Bohme ; J M Stutzmann ; J. FégerSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2001.
English descriptors
- KwdEn :
- Adrenergic Agents, Animals, Excitatory Amino Acid Antagonists (pharmacology), Functional Laterality, Male, Models, Animal, Neurons (drug effects), Neuroprotective Agents (pharmacology), Oxidopamine, Parkinson Disease (physiopathology), Parkinson Disease, Secondary (chemically induced), Rats, Rats, Sprague-Dawley, Riluzole (pharmacology), Sodium Channel Blockers (pharmacology), Substantia Nigra (drug effects), Substantia Nigra (pathology), Subthalamic Nucleus (drug effects), Subthalamic Nucleus (pathology), Subthalamic Nucleus (physiopathology).
- MESH :
- chemical , pharmacology : Excitatory Amino Acid Antagonists, Neuroprotective Agents, Riluzole, Sodium Channel Blockers.
- chemical : Adrenergic Agents, Oxidopamine.
- chemically induced : Parkinson Disease, Secondary.
- drug effects : Neurons, Substantia Nigra, Subthalamic Nucleus.
- pathology : Substantia Nigra, Subthalamic Nucleus.
- physiopathology : Parkinson Disease, Subthalamic Nucleus.
- Animals, Functional Laterality, Male, Models, Animal, Rats, Rats, Sprague-Dawley.
Abstract
An abnormal increase in the activity of neurons of the subthalamic nucleus is a key pathophysiological feature of Parkinson's disease. We sought to determine whether riluzole, a sodium channel inhibitor that interferes with glutamatergic neurotransmission, affects neuronal activity in this brain region. Intravenous administration of riluzole reduced the discharge rate of subthalamic neurons in rats with 6-OHDA-induced lesions of the midbrain. By contrast, no effect was observed in nonlesioned control animals. This property may contribute to the neuroprotective effects of riluzole in animal models of PD through the modulation of the glutamatergic inputs these neurons feedback to nigral dopaminergic neurons.
PubMed: 11748743
Links to Exploration step
pubmed:11748743Le document en format XML
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<author><name sortKey="Mouroux, M" sort="Mouroux, M" uniqKey="Mouroux M" first="M" last="Mouroux">M. Mouroux</name>
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<author><name sortKey="Bohme, G A" sort="Bohme, G A" uniqKey="Bohme G" first="G A" last="Bohme">G A Bohme</name>
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<author><name sortKey="Stutzmann, J M" sort="Stutzmann, J M" uniqKey="Stutzmann J" first="J M" last="Stutzmann">J M Stutzmann</name>
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<front><div type="abstract" xml:lang="en">An abnormal increase in the activity of neurons of the subthalamic nucleus is a key pathophysiological feature of Parkinson's disease. We sought to determine whether riluzole, a sodium channel inhibitor that interferes with glutamatergic neurotransmission, affects neuronal activity in this brain region. Intravenous administration of riluzole reduced the discharge rate of subthalamic neurons in rats with 6-OHDA-induced lesions of the midbrain. By contrast, no effect was observed in nonlesioned control animals. This property may contribute to the neuroprotective effects of riluzole in animal models of PD through the modulation of the glutamatergic inputs these neurons feedback to nigral dopaminergic neurons.</div>
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<Abstract><AbstractText>An abnormal increase in the activity of neurons of the subthalamic nucleus is a key pathophysiological feature of Parkinson's disease. We sought to determine whether riluzole, a sodium channel inhibitor that interferes with glutamatergic neurotransmission, affects neuronal activity in this brain region. Intravenous administration of riluzole reduced the discharge rate of subthalamic neurons in rats with 6-OHDA-induced lesions of the midbrain. By contrast, no effect was observed in nonlesioned control animals. This property may contribute to the neuroprotective effects of riluzole in animal models of PD through the modulation of the glutamatergic inputs these neurons feedback to nigral dopaminergic neurons.</AbstractText>
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