| First Author | Mikhaylova M | Year | 2018 |
| Journal | Neuron | Volume | 97 |
| Issue | 5 | Pages | 1110-1125.e14 |
| PubMed ID | 29478916 | Mgi Jnum | J:261692 |
| Mgi Id | MGI:6150592 | Doi | 10.1016/j.neuron.2018.01.046 |
| Citation | Mikhaylova M, et al. (2018) Caldendrin Directly Couples Postsynaptic Calcium Signals to Actin Remodeling in Dendritic Spines. Neuron 97(5):1110-1125.e14 |
| abstractText | Compartmentalization of calcium-dependent plasticity allows for rapid actin remodeling in dendritic spines. However, molecular mechanisms for the spatio-temporal regulation of filamentous actin (F-actin) dynamics by spinous Ca(2+)-transients are still poorly defined. We show that the postsynaptic Ca(2+) sensor caldendrin orchestrates nano-domain actin dynamics that are essential for actin remodeling in the early phase of long-term potentiation (LTP). Steep elevation in spinous [Ca(2+)]i disrupts an intramolecular interaction of caldendrin and allows cortactin binding. The fast on and slow off rate of this interaction keeps cortactin in an active conformation, and protects F-actin at the spine base against cofilin-induced severing. Caldendrin gene knockout results in higher synaptic actin turnover, altered nanoscale organization of spinous F-actin, defects in structural spine plasticity, LTP, and hippocampus-dependent learning. Collectively, the data indicate that caldendrin-cortactin directly couple [Ca(2+)]i to preserve a minimal F-actin pool that is required for actin remodeling in the early phase of LTP. |
