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© Christelle Durand
Microscopie d'un neurone. Le marquage jaune montre les synapses.
Publication : Journal of molecular neuroscience : MN

Targeted in vivo expression of nicotinic acetylcholine receptors in mouse brain using lentiviral expression vectors

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Journal of molecular neuroscience : MN - 01 Jan 2006

Molles BE, Maskos U, Pons S, Besson M, Guiard P, Guilloux JP, Evrard A, Cormier A, Mameli-Engvall M, Cloëz-Tayarani I, Nakatani H, Dufour N, Bemelmans AP, Mallet J, Cazala P, Gardier AM, David V, Faure P, Granon S, Changeux JP

Link to Pubmed [PMID] – 17192649

J. Mol. Neurosci. 2006;30(1-2):105-6

Nicotinic acetylcholine receptors (nAChRs) in the brain exhibit diverse functional properties and ubiquitous distribution. Yet, except for providing a receptor for the exogenously applied nicotine of tobacco products, their role in the normal functioning of the brain has remained elusive. We have used a lentiviral expression vector to re-express the beta2 subunit specifically in the ventral tegmental area (VTA) of beta2-/- mice. The viral vector efficiently expresses beta2- subunit protein leading to new nAChR-binding sites. VTA neurons transduced by the lentiviral vector are responsive to intravenous nicotine when analyzed using in vivo electrophysiology. Nicotine-induced dopamine release from the nucleus accumbens (NuAcc) was also restored in re-expressing beta2-/- mice. Intra-VTA injection of nicotine was found to be reinforcing in both wild-type and beta2-subunit re-expressing beta2-/- mice, but not in beta2-/- mice. Furthermore, in the absence of applied nicotine, the spontaneous slow exploratory behavior of the mice was restored, whereas fast navigation did not change. This latter behavioral analysis suggests a role for beta2* nAChR, specifically expressed in the VTA, in mammalian cognitive function.

https://www.ncbi.nlm.nih.gov/pubmed/17192649