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The Journal of Neuroscience, August 27, 2003, 23(21):7820-7829
 Previous Article | Next Article 
Subunit Composition of Functional Nicotinic Receptors in Dopaminergic Neurons Investigated with Knock-Out Mice
Nicolas Champtiaux,1
Cecilia Gotti,2
Matilde Cordero-Erausquin,1
Denis J. David,3
Cédric Przybylski,3
Clément Léna,1
Francesco Clementi,2
Milena Moretti,2
Francesco M. Rossi,1
Nicolas Le Novère,1
J. Michael McIntosh,4
Alain M. Gardier,3 and
Jean-Pierre Changeux1
1Laboratoire de Neurobiologie Moléculaire,
Centre National de la Recherche Scientifique Unité de Recherche
Associée 2182 "Récepteurs et Cognition," Institut
Pasteur, 75724 Paris Cedex 15, France, 2Consiglio
Nazionale delle Ricerche, Institute of Neuroscience, Section of Cellular and
Molecular Pharmacology, Department of Medical Pharmacology and Center of
Excellence on Neurodegenerative Diseases, University of Milan, 20129 Milan,
Italy, 3Laboratoire de Neuropharmacologie Equipe
Associée-Ministere de l'Education Nationale de la Recherche et de la
Technologie, Faculté de Pharmacie Institut Fédératif de
Recherche-Institut de Signalisation at Innovation Thérapeutique,
Institut de Signalisation et d'Innovation Thérapeutique,
Université Paris-Sud, F92296 Châtenay-Malabry cedex, France, and
4Departments of Psychiatry and Biology, University of
Utah, Salt Lake City, Utah 84112
Nicotinic acetylcholine receptors (nAChRs) expressed by dopaminergic (DA)
neurons have long been considered as potential therapeutic targets for the
treatment of several neuropsychiatric diseases, including nicotine and cocaine
addiction or Parkinson's disease. However, DA neurons express mRNAs coding for
most, if not all, neuronal nAChR subunits, and the subunit composition of
functional nAChRs has been difficult to establish. Immunoprecipitation
experiments performed on mouse striatal extracts allowed us to identify three
main types of heteromeric nAChRs ( 4 2*,
62*, and 462*) in DA
terminal fields. The functional relevance of these subtypes was then examined
by studying nicotine-induced DA release in striatal synaptosomes and recording
ACh-elicited currents in DA neurons from4, 6, 46,
and 2 knock-out mice. Our results establish that
62* nAChRs are functional and sensitive to
-conotoxin MII inhibition. These receptors are mainly located on DA
terminals and consistently do not contribute to DA release induced by systemic
nicotine administration, as evidenced by in vivo microdialysis. In
contrast, (non6)42* nAChRs represent the
majority of functional heteromeric nAChRs on DA neuronal soma. Thus, whereas a
combination of 62* and 42*
nAChRs may mediate the endogenous cholinergic modulation of DA release at the
terminal level, somato-dendritic (non6)42*
nAChRs most likely contribute to nicotine reinforcement.
Key words: dopamine; knock-out mice; mesencephalon; nicotinic acetylcholine receptors; striatum; -conotoxine MII
Received March 31, 2003;
revised June 24, 2003;
accepted July 7, 2003.
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S. L. Parker, Y. Fu, K. McAllen, J. Luo, J. M. McIntosh, J. M. Lindstrom, and B. M. Sharp
Up-Regulation of Brain Nicotinic Acetylcholine Receptors in the Rat during Long-Term Self-Administration of Nicotine: Disproportionate Increase of the {alpha}6 Subunit
Mol. Pharmacol.,
March 1, 2004;
65(3):
611 - 622.
[Abstract]
[Full Text]
[PDF]
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