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BookmarkScienceDaily (Mar. 15, 2009) — Prevalence of drug addiction (alcohol and illicit drug addiction only) in Europe is 9 million people and the annual cost is € 57 billion. Parkinson’s disease affects 1.2 million people and costs €11 billion each year.
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A research team -- Alban de Kerchove d’Exaerde, Research Associate FRS-FNRS and Serge Schiffmann in the Laboratory of Neurophysiology in the Faculté de médecine-Université Libre de Bruxelles (ULB) -- has made an important step toward the understanding of these diseases. Their work, published in Nature Neuroscience, has unravelled the unexpected role of a neuronal population in drug addiction and motor control.
Drug addiction and Parkinson’s disease induce, respectively, an excess or a deficit of the neurotransmitter dopamine. Dopamine is mainly secreted in a brain region -the striatum- involved in motivation, addiction and the control of movement. The striatum is mainly composed of two projection neuronal populations whose functional role has been difficult to assess and remains debated.
The ULB’s researchers have ablated one of these neuronal populations – the striatopallidal neurones - using a new transgenic mouse model: they demonstrated in the living transgenic mice that the striatopallidal neurones inhibit locomotor activity and the place preference and memorisation induced by drug taking. In other words, the mice with striatopallidal neurone ablation have higher locomotor activity and, more surprisingly, also higher and more persistent preference for the place where they have received an addictive drug.
By demonstrating the unexpected role of the striatopallidal neurones, the researchers open up interesting new therapeutic perspectives, aimed at the stimulation of this neuronal population in drug-dependent patients, or its inhibition in Parkinsonian patients.
Journal reference:
- Durieux, P.F., Bearzatto B, Guiducci, S., Buch, T., Waisman, A., Zoli, M., Schiffmann S.N. and de Kerchove d%u2019Exaerde, A. D2R striatopallidal neurons inhibit both locomotor and drug reward processes. Nature Neuroscience, 2009; DOI: 10.1038/nn.2286
