A phenotype for the α7 nicotinic acetylcholine receptor null mutant

The α7 nicotinic acetylcholine receptor (nAChR) is heavily expressed in the mammalian brain. On a molecular level, the α7 nAChR may have a diversity of functions, but it is not known if these molecular events translate into phenotypes. The null mutant mouse is viable and generally normal. Here, we r...

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Veröffentlicht in:Brain research Jg. 1023; H. 1; S. 41 - 47
Hauptverfasser: Morley, Barbara J., Rodriguez-Sierra, Jorge F.
Format: Journal Article
Sprache:Englisch
Veröffentlicht: London Elsevier B.V 01.10.2004
Amsterdam Elsevier
New York, NY
Schlagworte:
Biological and medical sciences
Cell receptors
Cell structures and functions
Endocrine
Fundamental and applied biological sciences. Psychology
Molecular and cellular biology
Monoamines receptors (catecholamine, serotonine, histamine, acetylcholine)
Mouse
Phenotype
α7 Nicotinic acetylcholine receptor
Endocrine
Phenotype
Mouse
Neurotransmitters, modulators, transporters, receptors
α7 Nicotinic acetylcholine receptor
Vertebrata
Mammalia
Rodentia
α7 nicotinic receptor
Neurotransmitter
Acetylcholine
Mutation
ISSN:0006-8993, 1872-6240
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Zusammenfassung:The α7 nicotinic acetylcholine receptor (nAChR) is heavily expressed in the mammalian brain. On a molecular level, the α7 nAChR may have a diversity of functions, but it is not known if these molecular events translate into phenotypes. The null mutant mouse is viable and generally normal. Here, we report a phenotype for the α7 nAChR null mutant mouse. The α7 nAChR is obligatory for the synchronization of an important biological rhythm, the female estrous cycle. The female null mutant mouse has asynchronous estrous cycles and a reduced number of surviving pups. Female null mutants also demonstrate a reliable diversity in phenotype, suggesting an interaction between environment and gene expression. Real-time RT-PCR measurements of the α7 mRNA expression in reproductive tissues of wild-type mice suggest that the ovulatory dysfunction in null mutants is probably central in origin.
ISSN:0006-8993
1872-6240
DOI:10.1016/j.brainres.2004.07.006