| First Author | Takahashi E | Year | 2010 |
| Journal | J Mol Neurosci | Volume | 41 |
| Issue | 2 | Pages | 223-9 |
| PubMed ID | 19609731 | Mgi Jnum | J:303766 |
| Mgi Id | MGI:6513690 | Doi | 10.1007/s12031-009-9216-5 |
| Citation | Takahashi E, et al. (2010) Interaction between Ca(v)2.1alpha (1) and CaMKII in Ca (v)2.1alpha (1) mutant mice, Rolling Nagoya. J Mol Neurosci 41(2):223-9 |
| abstractText | It has been reported earlier that interactions between Ca(v)2.1alpha(1) and calcium/calmodulin-dependent protein kinase II (CaMKII) in the presynaptic fraction and between the NMDA receptor subunit NR2B and CaMKII in the postsynaptic density (PSD) fraction are important for neuronal function. Ca(v)2.1alpha(1), CaMKII, and NR2B are predominantly expressed in the hippocampus. To examine the above interactions and CaMKII activity in the hippocampal presynapse and PSD of Rolling Nagoya mice carrying a mutation in Ca(v)2.1alpha(1) subunit, we performed immunoprecipitation and Western blot analyses. In the presynapse, the interaction between Ca(v)2.1alpha(1) and CaMKII and the phosphorylation of CaMKII (at Thr286) and its substrate Synapsin I (at Ser603) were decreased in mutant mice compared to wild-type mice. In the PSD, a similar pattern was observed for the interaction between NR2B and CaMKII and the phosphorylation of CaMKII (at Thr286) and its substrate AMPA receptor subunit glutamate receptor 1 (at Ser831) between mutant and wild-type mice. Our data indicate that disruption of the interaction between Ca(v)2.1alpha(1) and CaMKII may down-regulate presynaptic CaMKII activity and that Rolling Nagoya mice would be a useful model for examining presynaptic function. |
