Riluzole reduces hyperactivity of subthalamic neurons induced by unilateral 6-OHDA lesion in the rat brain

Authors

  • Oum-Kaltoum Hassani PhD,

    1. Laboratoire de Pharmacologie, Faculté de Sciences Pharmaceutiques et Biologiques, Université René Descartes, Paris, France
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  • Mireille Mouroux PhD,

    1. Laboratoire de Pharmacologie, Faculté de Sciences Pharmaceutiques et Biologiques, Université René Descartes, Paris, France
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  • Georg Andrees Bohme PharmD, PhD,

    1. Aventis Pharma France S.A., Neurodegenerative Disease Group, Centre de Recherches de Paris, France
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  • Jean-Marie Stutzmann PhD,

    1. Aventis Pharma France S.A., Neurodegenerative Disease Group, Centre de Recherches de Paris, France
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  • Jean Féger PhD

    Corresponding author
    1. Laboratoire de Pharmacologie, Faculté de Sciences Pharmaceutiques et Biologiques, Université René Descartes, Paris, France
    2. INSERM U-289, Hopital de la Salpêtrière, Paris, France
    • INSERM U-289, Hôpital de la Salpêtrière, 47 Boulevard de l'Hôpital, 75651 Paris Cedex 13, France
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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. © 2001 Movement Disorder Society.

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