Abstract
The dopaminergic receptor D1 activates and the muscarinic acetylcholine receptor (mAChR) M4 inhibits adenylyl cyclase (AC) and thereby cAMP production through the trimeric Gαs and Gαi/o proteins, respectively (Wess et al, 2007). D1 and M4 are coexpressed in striatal output neurons, where M4 antagonizes D1 signalling as recently pinpointed by conditional M4 knockout in D1-expressing neurons (Jeon et al, 2010). Closely following on the heels of this article, Guo et al (2010) report in this issue that CaMKII binds and phosphorylates M4 upon Ca2+ influx to augment the antagonistic action of M4 on D1 signalling and on D1-mediated, cocaine-triggered hyperlocomotion.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 1943-1945 |
| Number of pages | 3 |
| Journal | EMBO Journal |
| Volume | 29 |
| Issue number | 12 |
| DOIs | |
| State | Published - Jun 16 2010 |
ASJC Scopus subject areas
- Molecular Biology
- Biochemistry, Genetics and Molecular Biology(all)
- Immunology and Microbiology(all)
- Neuroscience(all)
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Stein, I. S., & Hell, J. W. (2010). CaMKII hunkers down on the muscarinic M4 receptor to help curb cocaine-induced hyperlocomotion. EMBO Journal, 29(12), 1943-1945. https://doi.org/10.1038/emboj.2010.105