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

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Title: Nicotine reinforcement and cognition restored by targeted expression of nicotinic receptors.
Authors: Maskos, U., Molles, B. E., Pons, S., Besson, M., Guiard, B. P., Guilloux, J.-P., Evrard, A., Cazala, P., Cormier, A., Mameli-Engvall, M., Dufour, N., Cloëz-Tayarani, I., Bemelmans, A.-P., Mallet, J., Gardier, A. M., David, V., Faure, P., Granon, S., Changeux, J.-P.
Source: Nature. 7/7/2005, Vol. 436 Issue 7047, p103-107. 5p.
Subjects: Nicotine, Pyridine, Cognition, Nicotinic receptors, Cholinergic receptors, Neurotransmitter receptors
Abstract: Worldwide, 100 million people are expected to die this century from the consequences of nicotine addiction, but nicotine is also known to enhance cognitive performance. Identifying the molecular mechanisms involved in nicotine reinforcement and cognition is a priority and requires the development of new in vivo experimental paradigms. The ventral tegmental area (VTA) of the midbrain is thought to mediate the reinforcement properties of many drugs of abuse. Here we specifically re-expressed the β2-subunit of the nicotinic acetylcholine receptor (nAChR) by stereotaxically injecting a lentiviral vector into the VTA of mice carrying β2-subunit deletions. We demonstrate the efficient re-expression of electrophysiologically responsive, ligand-binding nicotinic acetylcholine receptors in dopamine-containing neurons of the VTA, together with the recovery of nicotine-elicited dopamine release and nicotine self-administration. We also quantified exploratory behaviours of the mice, and showed that β2-subunit re-expression restored slow exploratory behaviour (a measure of cognitive function) to wild-type levels, but did not affect fast navigation behaviour. We thus demonstrate the sufficient role of the VTA in both nicotine reinforcement and endogenous cholinergic regulation of cognitive functions. [ABSTRACT FROM AUTHOR]
Copyright of Nature is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Psychology and Behavioral Sciences Collection
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  Data: <searchLink fieldCode="AR" term="%22Maskos%2C+U%2E%22">Maskos, U.</searchLink><br /><searchLink fieldCode="AR" term="%22Molles%2C+B%2E+E%2E%22">Molles, B. E.</searchLink><br /><searchLink fieldCode="AR" term="%22Pons%2C+S%2E%22">Pons, S.</searchLink><br /><searchLink fieldCode="AR" term="%22Besson%2C+M%2E%22">Besson, M.</searchLink><br /><searchLink fieldCode="AR" term="%22Guiard%2C+B%2E+P%2E%22">Guiard, B. P.</searchLink><br /><searchLink fieldCode="AR" term="%22Guilloux%2C+J%2E-P%2E%22">Guilloux, J.-P.</searchLink><br /><searchLink fieldCode="AR" term="%22Evrard%2C+A%2E%22">Evrard, A.</searchLink><br /><searchLink fieldCode="AR" term="%22Cazala%2C+P%2E%22">Cazala, P.</searchLink><br /><searchLink fieldCode="AR" term="%22Cormier%2C+A%2E%22">Cormier, A.</searchLink><br /><searchLink fieldCode="AR" term="%22Mameli-Engvall%2C+M%2E%22">Mameli-Engvall, M.</searchLink><br /><searchLink fieldCode="AR" term="%22Dufour%2C+N%2E%22">Dufour, N.</searchLink><br /><searchLink fieldCode="AR" term="%22Cloëz-Tayarani%2C+I%2E%22">Cloëz-Tayarani, I.</searchLink><br /><searchLink fieldCode="AR" term="%22Bemelmans%2C+A%2E-P%2E%22">Bemelmans, A.-P.</searchLink><br /><searchLink fieldCode="AR" term="%22Mallet%2C+J%2E%22">Mallet, J.</searchLink><br /><searchLink fieldCode="AR" term="%22Gardier%2C+A%2E+M%2E%22">Gardier, A. M.</searchLink><br /><searchLink fieldCode="AR" term="%22David%2C+V%2E%22">David, V.</searchLink><br /><searchLink fieldCode="AR" term="%22Faure%2C+P%2E%22">Faure, P.</searchLink><br /><searchLink fieldCode="AR" term="%22Granon%2C+S%2E%22">Granon, S.</searchLink><br /><searchLink fieldCode="AR" term="%22Changeux%2C+J%2E-P%2E%22">Changeux, J.-P.</searchLink>
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  Data: <searchLink fieldCode="DE" term="%22Nicotine%22">Nicotine</searchLink><br /><searchLink fieldCode="DE" term="%22Pyridine%22">Pyridine</searchLink><br /><searchLink fieldCode="DE" term="%22Cognition%22">Cognition</searchLink><br /><searchLink fieldCode="DE" term="%22Nicotinic+receptors%22">Nicotinic receptors</searchLink><br /><searchLink fieldCode="DE" term="%22Cholinergic+receptors%22">Cholinergic receptors</searchLink><br /><searchLink fieldCode="DE" term="%22Neurotransmitter+receptors%22">Neurotransmitter receptors</searchLink>
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  Data: Worldwide, 100 million people are expected to die this century from the consequences of nicotine addiction, but nicotine is also known to enhance cognitive performance. Identifying the molecular mechanisms involved in nicotine reinforcement and cognition is a priority and requires the development of new in vivo experimental paradigms. The ventral tegmental area (VTA) of the midbrain is thought to mediate the reinforcement properties of many drugs of abuse. Here we specifically re-expressed the β2-subunit of the nicotinic acetylcholine receptor (nAChR) by stereotaxically injecting a lentiviral vector into the VTA of mice carrying β2-subunit deletions. We demonstrate the efficient re-expression of electrophysiologically responsive, ligand-binding nicotinic acetylcholine receptors in dopamine-containing neurons of the VTA, together with the recovery of nicotine-elicited dopamine release and nicotine self-administration. We also quantified exploratory behaviours of the mice, and showed that β2-subunit re-expression restored slow exploratory behaviour (a measure of cognitive function) to wild-type levels, but did not affect fast navigation behaviour. We thus demonstrate the sufficient role of the VTA in both nicotine reinforcement and endogenous cholinergic regulation of cognitive functions. [ABSTRACT FROM AUTHOR]
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  Data: <i>Copyright of Nature is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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