| First Author | Tu X | Year | 2020 |
| Journal | Sci Rep | Volume | 10 |
| Issue | 1 | Pages | 1777 |
| PubMed ID | 32019972 | Mgi Jnum | J:298476 |
| Mgi Id | MGI:6480159 | Doi | 10.1038/s41598-020-58610-6 |
| Citation | Tu X, et al. (2020) Rac1 is a downstream effector of PKCalpha in structural synaptic plasticity. Sci Rep 10(1):1777 |
| abstractText | Structural and functional plasticity of dendritic spines is the basis of animal learning. The rapid remodeling of actin cytoskeleton is associated with spine enlargement and shrinkage, which are essential for structural plasticity. The calcium-dependent protein kinase C isoform, PKCalpha, has been suggested to be critical for this actin-dependent plasticity. However, mechanisms linking PKCalpha and structural plasticity of spines are unknown. Here, we examine the spatiotemporal activation of actin regulators, including small GTPases Rac1, Cdc42 and Ras, in the presence or absence of PKCalpha during single-spine structural plasticity. Removal of PKCalpha expression in the postsynapse attenuated Rac1 activation during structural plasticity without affecting Ras or Cdc42 activity. Moreover, disruption of a PDZ binding domain within PKCalpha led to impaired Rac1 activation and deficits in structural spine remodeling. These results demonstrate that PKCalpha positively regulates the activation of Rac1 during structural plasticity. |
