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The Journal of Neuroscience, February 15, 2002, 22(4):1208-1217
Distribution and Pharmacology of  6-Containing Nicotinic
Acetylcholine Receptors Analyzed with Mutant Mice
Nicolas
Champtiaux1,
Zhi-Yan
Han1,
Alain
Bessis2,
Francesco Mattia
Rossi1,
Michele
Zoli1, 3,
Lisa
Marubio4,
J. Michael
McIntosh5, and
Jean-Pierre
Changeux1
1 Laboratoire de Neurobiologie Moléculaire,
Centre National de la Recherche Scientifique, Unité de Recherche
Associée 2182, Récepteurs et Cognition, Institut Pasteur
75724 Paris, Cedex 15, France, 2 Laboratoire de Biologie
Cellulaire de la Synapse, Ecole Normale Supérieure, 75005 Paris,
France, 3 Department of Biomedical Sciences, Section of
Physiology, University of Modena and Reggio Emilia, 41100 Modena,
Italy, 4 Department of Molecular and Human Genetics, Baylor
College of Medicine, Houston, Texas 77030, and 5 Department
of Biology, University of Utah, Salt Lake City, Utah 84112
The  6 subunit of the nicotinic acetylcholine receptor (nAChR) is
expressed at very high levels in dopaminergic (DA) neurons. However,
because of the lack of pharmacological tools selective for
6-containing nAChRs, the role of this subunit in the etiology of
nicotine addiction remains unknown. To provide new tools to investigate
this issue, we generated an 6 nAChR knock-out mouse. Homozygous null
mutants (6 /) did not exhibit any gross neurological or
behavioral deficits. A careful anatomic and molecular examination of
6/ mouse brains demonstrated the absence of developmental alterations in these animals, especially in the visual and dopaminergic pathways, where the 6 subunit is normally expressed at the highest levels. On the other hand, receptor autoradiography revealed a decrease
in [3H]nicotine,
[3H]epibatidine, and
[3H]cytisine high-affinity binding in the terminal
fields of retinal ganglion cells of 6/ animals, whereas
high-affinity [125I]-conotoxinMII (CtxMII)
binding completely disappeared in the brain. Moreover, inhibition of
[3H]epibatidine binding on striatal membranes,
using unlabeled CtxMII or cytisine, revealed the absence of
CtxMII-sensitive and cytisine-resistant [3H]epibatidine binding sites in 6/ mice,
although the total amount of binding was unchanged. Because CtxMII,
a toxin formerly thought to be specific for 3 2-containing nAChRs,
is known to partially inhibit nicotine-induced dopamine release, these
results support the conclusion that 6 rather than 3 is the
partner of 2 in the nicotinic modulation of DA neurons. They further
show that 6/ mice might be useful tools to understand the
mechanisms of nicotine addiction, although some developmental
compensation might occur in these mice.
Key words:
nicotinic acetylcholine receptor; knock-out; 6
subunit; -conotoxinMII; dopaminergic system; visual system
Copyright © 2002 Society for Neuroscience 0270-6474/02/2241208-10$05.00/0
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P. Whiteaker, C. G. Peterson, W. Xu, J. M. McIntosh, R. Paylor, A. L. Beaudet, A. C. Collins, and M. J. Marks
Involvement of the alpha 3 Subunit in Central Nicotinic Binding Populations
J. Neurosci.,
April 1, 2002;
22(7):
2522 - 2529.
[Abstract]
[Full Text]
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