| First Author | Incontro S | Year | 2018 |
| Journal | Nat Commun | Volume | 9 |
| Issue | 1 | Pages | 2069 |
| PubMed ID | 29802289 | Mgi Jnum | J:262916 |
| Mgi Id | MGI:6161049 | Doi | 10.1038/s41467-018-04439-7 |
| Citation | Incontro S, et al. (2018) The CaMKII/NMDA receptor complex controls hippocampal synaptic transmission by kinase-dependent and independent mechanisms. Nat Commun 9(1):2069 |
| abstractText | CaMKII is one of the most studied synaptic proteins, but many critical issues regarding its role in synaptic function remain unresolved. Using a CRISPR-based system to delete CaMKII and replace it with mutated forms in single neurons, we have rigorously addressed its various synaptic roles. In brief, basal AMPAR and NMDAR synaptic transmission both require CaMKIIalpha, but not CaMKIIbeta, indicating that, even in the adult, synaptic transmission is determined by the ongoing action of CaMKIIalpha. While AMPAR transmission requires kinase activity, NMDAR transmission does not, implying a scaffolding role for the CaMKII protein instead. LTP is abolished in the absence of CaMKIIalpha and/or CaMKIIbeta and with an autophosphorylation impaired CaMKIIalpha (T286A). With the exception of NMDAR synaptic currents, all aspects of CaMKIIalpha signaling examined require binding to the NMDAR, emphasizing the essential role of this receptor as a master synaptic signaling hub. |
