Muscarinic receptors are affected by corticotropin-releasing hormone and c-fos gene disruptions: is there a mutual connection to adrenoceptors?
Language English Country United States Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
17192632
DOI
10.1385/jmn:30:1:69
PII: JMN:30:1:69
Knihovny.cz E-resources
- MeSH
- Receptors, Adrenergic physiology MeSH
- Restraint, Physical MeSH
- Genes, fos * MeSH
- Corticotropin-Releasing Hormone deficiency genetics physiology MeSH
- Mice, Knockout MeSH
- Mice MeSH
- Stress, Psychological physiopathology MeSH
- Receptors, Muscarinic physiology MeSH
- Animals MeSH
- Check Tag
- Mice MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Receptors, Adrenergic MeSH
- Corticotropin-Releasing Hormone MeSH
- Receptors, Muscarinic MeSH
In the last decade, progress in gene disruption technology has allowed the study of the effects of the single-gene knockout (KO) on different molecules involved in the signaling cascade activated via muscarinic receptors. Many KO mice targeting muscarinic receptors have been developed, that is, all (M1-M5) muscarinic receptor KO mice (Wess, 2003) and acetylcholinesterase (AChE) KO mice(Xie et al., 2000). Recently, we have shown that these (AChE-/-) mice not only reveal changes in the number of muscarinic receptors in the heart, lung, cortex, and cerebellum but also in the number of adrenoceptors (Teplicky et al., 2004). Next, we studied whether the disruption of corticotropin-releasing hormone (CRH) or c-Fos could affect the properties of muscarinic receptors and adrenoceptors in the lungs and hearts of mice. The effects of immobilization stress in CRH KO animals were also studied.
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