Riluzole reduces hyperactivity of subthalamic neurons induced by unilateral 6-OHDA lesion in the rat brain
Identifieur interne : 000289 ( PascalFrancis/Curation ); précédent : 000288; suivant : 000290Riluzole reduces hyperactivity of subthalamic neurons induced by unilateral 6-OHDA lesion in the rat brain
Auteurs : Oum-Kaltoum Hassani [France] ; Mireille Mouroux [France] ; Georg Andrees Bohme [France] ; Jean-Marie Stutzmann [France] ; Jean Feger [France]Source :
- Movement disorders [ 0885-3185 ] ; 2001.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Sodium.
English descriptors
- KwdEn :
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.
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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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<s5>38</s5>
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<fC07 i1="06" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>38</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Encéphale pathologie</s0>
<s5>39</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>39</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>39</s5>
</fC07>
<fC07 i1="08" i2="X" l="FRE"><s0>Extrapyramidal syndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="08" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="08" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="09" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>41</s5>
</fC07>
<fC07 i1="09" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>41</s5>
</fC07>
<fC07 i1="09" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>41</s5>
</fC07>
<fC07 i1="10" i2="X" l="FRE"><s0>Encéphale</s0>
<s5>53</s5>
</fC07>
<fC07 i1="10" i2="X" l="ENG"><s0>Brain (vertebrata)</s0>
<s5>53</s5>
</fC07>
<fC07 i1="10" i2="X" l="SPA"><s0>Encéfalo</s0>
<s5>53</s5>
</fC07>
<fN21><s1>098</s1>
</fN21>
<fN82><s1>PSI</s1>
</fN82>
</pA>
</standard>
</inist>
</record>
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