| First Author | Sugawara T | Year | 2017 |
| Journal | Proc Natl Acad Sci U S A | Volume | 114 |
| Issue | 26 | Pages | E5256-E5265 |
| PubMed ID | 28607044 | Mgi Jnum | J:244888 |
| Mgi Id | MGI:5913667 | Doi | 10.1073/pnas.1617270114 |
| Citation | Sugawara T, et al. (2017) Regulation of spinogenesis in mature Purkinje cells via mGluR/PKC-mediated phosphorylation of CaMKIIbeta. Proc Natl Acad Sci U S A 114(26):E5256-E5265 |
| abstractText | Dendritic spines of Purkinje cells form excitatory synapses with parallel fiber terminals, which are the primary sites for cerebellar synaptic plasticity. Nevertheless, how density and morphology of these spines are properly maintained in mature Purkinje cells is not well understood. Here we show an activity-dependent mechanism that represses excessive spine development in mature Purkinje cells. We found that CaMKIIbeta promotes spine formation and elongation in Purkinje cells through its F-actin bundling activity. Importantly, activation of group I mGluR, but not AMPAR, triggers PKC-mediated phosphorylation of CaMKIIbeta, which results in dissociation of the CaMKIIbeta/F-actin complex. Defective function of the PKC-mediated CaMKIIbeta phosphorylation promotes excess F-actin bundling and leads to abnormally numerous and elongated spines in mature IP3R1-deficient Purkinje cells. Thus, our data suggest that phosphorylation of CaMKIIbeta through the mGluR/IP3R1/PKC signaling pathway represses excessive spine formation and elongation in mature Purkinje cells. |
