Rac1 is a downstream effector of PKCα in structural synaptic plasticity

Abstract

Structural and functional plasticity of dendritic spines is the basis of animal learning. The calcium-dependent protein kinase C isoform, PKC, has been suggested to be critical for this actin-dependent plasticity. However, mechanisms linking PKC 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 PKC during single-spine structural plasticity. Removal of PKC expression in the postsynapse attenuated Rac1 activation during structural plasticity without affecting Ras or Cdc42 activity. Moreover, disruption of a PDZ binding domain within PKC led to impaired Rac1 activation and deficits in structural spine remodeling. These results demonstrate that PKC positively regulates the activation of Rac1 during structural plasticity.