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Uwe Maskos

Researcher at Pasteur Institute

Publications -  107
Citations -  4921

Uwe Maskos is an academic researcher from Pasteur Institute. The author has contributed to research in topics: Nicotinic agonist & Nicotine. The author has an hindex of 33, co-authored 94 publications receiving 4324 citations. Previous affiliations of Uwe Maskos include Centre national de la recherche scientifique & University of Paris.

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Nicotine reinforcement and cognition restored by targeted expression of nicotinic receptors.

TL;DR: The efficient re-expression of electrophysiologically responsive, ligand-binding nicotinic acetylcholine receptors in dopamine-containing neurons of the VTA is demonstrated, together with the recovery of nicotine-elicited dopamine release and nicotine self-administration.
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Crucial Role of α4 and α6 Nicotinic Acetylcholine Receptor Subunits from Ventral Tegmental Area in Systemic Nicotine Self-Administration

TL;DR: The necessary and sufficient role of α4β2- and α6 β2-subunit containing nicotinic receptors, but not α7*-nAChRs, present in cell bodies of the VTA, and their axons, for systemic nicotine reinforcement in drug-naive mice are defined.
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Hierarchical Control of Dopamine Neuron-Firing Patterns by Nicotinic Receptors

TL;DR: A hierarchical control of dopaminergic neuron firing patterns by nAChRs is suggested: activation of beta2*-nAChR switches cells from a resting to an excited state, whereas activation of alpha7*-magnifying lens finely tunes the latter state but only once beta2-n AChRs have been activated.
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Aversion to Nicotine Is Regulated by the Balanced Activity of β4 and α5 Nicotinic Receptor Subunits in the Medial Habenula

TL;DR: This study provides insights into α3β4α5 receptor-mediated mechanisms contributing to nicotine consumption, and identifies the MHb as a critical element in the circuitry controlling nicotine-dependent phenotypes.
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Role of the nicotinic acetylcholine receptor in Alzheimer's disease pathology and treatment

TL;DR: How Aβ activates or inhibits nAChRs, and how this interaction contributes to AD pathology is discussed, and the potential role of nA cholinergic tone and acetylcholine receptor families as therapeutic targets are discussed.